Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel
BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathio...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wen Yu [verfasserIn] Ying Liao [verfasserIn] Yaqian Huang [verfasserIn] Selena Y. Chen [verfasserIn] Yan Sun [verfasserIn] Chufan Sun [verfasserIn] Yuming Wu [verfasserIn] Chaoshu Tang [verfasserIn] Junbao Du [verfasserIn] Hongfang Jin [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
transient receptor potential cation channel subfamily V member 1 |
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| Übergeordnetes Werk: |
In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease - Wiley, 2012, 6(2017), 5 |
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| Übergeordnetes Werk: |
volume:6 ; year:2017 ; number:5 |
| Links: |
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| DOI / URN: |
10.1161/JAHA.116.004971 |
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| Katalog-ID: |
DOAJ051202344 |
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| 245 | 1 | 0 | |a Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel |
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| 520 | |a BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. | ||
| 650 | 4 | |a carotid sinus baroreceptor | |
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| 700 | 0 | |a Yan Sun |e verfasserin |4 aut | |
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| 700 | 0 | |a Junbao Du |e verfasserin |4 aut | |
| 700 | 0 | |a Hongfang Jin |e verfasserin |4 aut | |
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10.1161/JAHA.116.004971 doi (DE-627)DOAJ051202344 (DE-599)DOAJd511bc44f2434dc4b016b810b769a4af DE-627 ger DE-627 rakwb eng RC666-701 Wen Yu verfasserin aut Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. carotid sinus baroreceptor hydrogen sulfide hypertension transient receptor potential cation channel subfamily V member 1 Diseases of the circulatory (Cardiovascular) system Ying Liao verfasserin aut Yaqian Huang verfasserin aut Selena Y. Chen verfasserin aut Yan Sun verfasserin aut Chufan Sun verfasserin aut Yuming Wu verfasserin aut Chaoshu Tang verfasserin aut Junbao Du verfasserin aut Hongfang Jin verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 6(2017), 5 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:6 year:2017 number:5 https://doi.org/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/article/d511bc44f2434dc4b016b810b769a4af kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2017 5 |
| spelling |
10.1161/JAHA.116.004971 doi (DE-627)DOAJ051202344 (DE-599)DOAJd511bc44f2434dc4b016b810b769a4af DE-627 ger DE-627 rakwb eng RC666-701 Wen Yu verfasserin aut Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. carotid sinus baroreceptor hydrogen sulfide hypertension transient receptor potential cation channel subfamily V member 1 Diseases of the circulatory (Cardiovascular) system Ying Liao verfasserin aut Yaqian Huang verfasserin aut Selena Y. Chen verfasserin aut Yan Sun verfasserin aut Chufan Sun verfasserin aut Yuming Wu verfasserin aut Chaoshu Tang verfasserin aut Junbao Du verfasserin aut Hongfang Jin verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 6(2017), 5 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:6 year:2017 number:5 https://doi.org/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/article/d511bc44f2434dc4b016b810b769a4af kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2017 5 |
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10.1161/JAHA.116.004971 doi (DE-627)DOAJ051202344 (DE-599)DOAJd511bc44f2434dc4b016b810b769a4af DE-627 ger DE-627 rakwb eng RC666-701 Wen Yu verfasserin aut Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. carotid sinus baroreceptor hydrogen sulfide hypertension transient receptor potential cation channel subfamily V member 1 Diseases of the circulatory (Cardiovascular) system Ying Liao verfasserin aut Yaqian Huang verfasserin aut Selena Y. Chen verfasserin aut Yan Sun verfasserin aut Chufan Sun verfasserin aut Yuming Wu verfasserin aut Chaoshu Tang verfasserin aut Junbao Du verfasserin aut Hongfang Jin verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 6(2017), 5 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:6 year:2017 number:5 https://doi.org/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/article/d511bc44f2434dc4b016b810b769a4af kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2017 5 |
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10.1161/JAHA.116.004971 doi (DE-627)DOAJ051202344 (DE-599)DOAJd511bc44f2434dc4b016b810b769a4af DE-627 ger DE-627 rakwb eng RC666-701 Wen Yu verfasserin aut Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. carotid sinus baroreceptor hydrogen sulfide hypertension transient receptor potential cation channel subfamily V member 1 Diseases of the circulatory (Cardiovascular) system Ying Liao verfasserin aut Yaqian Huang verfasserin aut Selena Y. Chen verfasserin aut Yan Sun verfasserin aut Chufan Sun verfasserin aut Yuming Wu verfasserin aut Chaoshu Tang verfasserin aut Junbao Du verfasserin aut Hongfang Jin verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 6(2017), 5 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:6 year:2017 number:5 https://doi.org/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/article/d511bc44f2434dc4b016b810b769a4af kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2017 5 |
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10.1161/JAHA.116.004971 doi (DE-627)DOAJ051202344 (DE-599)DOAJd511bc44f2434dc4b016b810b769a4af DE-627 ger DE-627 rakwb eng RC666-701 Wen Yu verfasserin aut Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. carotid sinus baroreceptor hydrogen sulfide hypertension transient receptor potential cation channel subfamily V member 1 Diseases of the circulatory (Cardiovascular) system Ying Liao verfasserin aut Yaqian Huang verfasserin aut Selena Y. Chen verfasserin aut Yan Sun verfasserin aut Chufan Sun verfasserin aut Yuming Wu verfasserin aut Chaoshu Tang verfasserin aut Junbao Du verfasserin aut Hongfang Jin verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 6(2017), 5 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:6 year:2017 number:5 https://doi.org/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/article/d511bc44f2434dc4b016b810b769a4af kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.116.004971 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2017 5 |
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Wen Yu @@aut@@ Ying Liao @@aut@@ Yaqian Huang @@aut@@ Selena Y. Chen @@aut@@ Yan Sun @@aut@@ Chufan Sun @@aut@@ Yuming Wu @@aut@@ Chaoshu Tang @@aut@@ Junbao Du @@aut@@ Hongfang Jin @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ051202344</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308160503.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1161/JAHA.116.004971</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ051202344</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJd511bc44f2434dc4b016b810b769a4af</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Wen Yu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. 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Wen Yu |
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Wen Yu misc RC666-701 misc carotid sinus baroreceptor misc hydrogen sulfide misc hypertension misc transient receptor potential cation channel subfamily V member 1 misc Diseases of the circulatory (Cardiovascular) system Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel |
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RC666-701 Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel carotid sinus baroreceptor hydrogen sulfide hypertension transient receptor potential cation channel subfamily V member 1 |
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misc RC666-701 misc carotid sinus baroreceptor misc hydrogen sulfide misc hypertension misc transient receptor potential cation channel subfamily V member 1 misc Diseases of the circulatory (Cardiovascular) system |
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Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel |
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Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel |
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Wen Yu Ying Liao Yaqian Huang Selena Y. Chen Yan Sun Chufan Sun Yuming Wu Chaoshu Tang Junbao Du Hongfang Jin |
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endogenous hydrogen sulfide enhances carotid sinus baroreceptor sensitivity by activating the transient receptor potential cation channel subfamily v member 1 (trpv1) channel |
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RC666-701 |
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Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel |
| abstract |
BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. |
| abstractGer |
BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. |
| abstract_unstemmed |
BackgroundWe aimed to investigate the regulatory effects of hydrogen sulfide (H2S) on carotid sinus baroreceptor sensitivity and its mechanisms. Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. Meanwhile, the downregulation of TRPV1 protein was demonstrated in the carotid sinus; however, H2S reduced systolic blood pressure but enhanced carotid sinus baroreceptor sensitivity in SHRs, along with TRPV1 upregulation in the carotid sinus. In contrast, hydroxylamine significantly increased the systolic blood pressure of Wistar‐Kyoto rats, along with decreased carotid sinus baroreceptor sensitivity and reduced TRPV1 protein expression in the carotid sinus. Furthermore, H2S‐induced enhancement of carotid sinus baroreceptor sensitivity of SHRs could be amplified by capsaicin but reduced by capsazepine. Moreover, H2S facilitated S‐sulfhydration of TRPV1 protein in the carotid sinus of SHRs and Wistar‐Kyoto rats. ConclusionsH2S regulated blood pressure via an increase in TRPV1 protein expression and its activity to enhance carotid sinus baroreceptor sensitivity. |
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Endogenous Hydrogen Sulfide Enhances Carotid Sinus Baroreceptor Sensitivity by Activating the Transient Receptor Potential Cation Channel Subfamily V Member 1 (TRPV1) Channel |
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https://doi.org/10.1161/JAHA.116.004971 https://doaj.org/article/d511bc44f2434dc4b016b810b769a4af https://www.ahajournals.org/doi/10.1161/JAHA.116.004971 https://doaj.org/toc/2047-9980 |
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Ying Liao Yaqian Huang Selena Y. Chen Yan Sun Chufan Sun Yuming Wu Chaoshu Tang Junbao Du Hongfang Jin |
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Ying Liao Yaqian Huang Selena Y. Chen Yan Sun Chufan Sun Yuming Wu Chaoshu Tang Junbao Du Hongfang Jin |
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10.1161/JAHA.116.004971 |
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2024-07-03T18:58:35.904Z |
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Methods and ResultsMale Wistar‐Kyoto rats and spontaneously hypertensive rats (SHRs) were used in the experiment and were given an H2S donor or a cystathionine‐β‐synthase inhibitor, hydroxylamine, for 8 weeks. Systolic blood pressure and the cystathionine‐β‐synthase/H2S pathway in carotid sinus were detected. Carotid sinus baroreceptor sensitivity and the functional curve of the carotid baroreceptor were analyzed using the isolated carotid sinus perfusion technique. Effects of H2S on transient receptor potential cation channel subfamily V member 1 (TRPV1) expression and S‐sulfhydration were detected. In SHRs, systolic blood pressure was markedly increased, but the cystathionine‐β‐synthase/H2S pathway in the carotid sinus was downregulated in comparison to that of Wistar‐Kyoto rats. Carotid sinus baroreceptor sensitivity in SHRs was reduced, demonstrated by the right and upward shift of the functional curve of the carotid baroreceptor. 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