P.27 Mechanisms of NADPH Oxidase Participation in the Regulation of Diaphragm Artery Contractile Responses
Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscl...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Borzykh, Anna [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Schlagwörter: |
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| Anmerkung: |
© Association for Research into Arterial Structure and Physiology 2020 |
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| Übergeordnetes Werk: |
Enthalten in: Artery research - Amsterdam : Atlantis Press, 2006, 26(2020), Suppl 1 vom: Dez., Seite S50-S50 |
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| Übergeordnetes Werk: |
volume:26 ; year:2020 ; number:Suppl 1 ; month:12 ; pages:S50-S50 |
| Links: |
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| DOI / URN: |
10.2991/artres.k.201209.040 |
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SPR054760550 |
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| 520 | |a Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). | ||
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10.2991/artres.k.201209.040 doi (DE-627)SPR054760550 (SPR)artres.k.201209.040-e DE-627 ger DE-627 rakwb eng Borzykh, Anna verfasserin aut P.27 Mechanisms of NADPH Oxidase Participation in the Regulation of Diaphragm Artery Contractile Responses 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Association for Research into Arterial Structure and Physiology 2020 Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). Artery (dpeaa)DE-He213 diaphragm (dpeaa)DE-He213 NADPH oxidase (dpeaa)DE-He213 Kuzmin, Ilya aut Vinogradova, Olga aut Tarasova, Olga aut Enthalten in Artery research Amsterdam : Atlantis Press, 2006 26(2020), Suppl 1 vom: Dez., Seite S50-S50 (DE-627)534057489 (DE-600)2364789-9 1876-4401 nnns volume:26 year:2020 number:Suppl 1 month:12 pages:S50-S50 https://dx.doi.org/10.2991/artres.k.201209.040 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2014 GBV_ILN_2068 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 26 2020 Suppl 1 12 S50-S50 |
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10.2991/artres.k.201209.040 doi (DE-627)SPR054760550 (SPR)artres.k.201209.040-e DE-627 ger DE-627 rakwb eng Borzykh, Anna verfasserin aut P.27 Mechanisms of NADPH Oxidase Participation in the Regulation of Diaphragm Artery Contractile Responses 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Association for Research into Arterial Structure and Physiology 2020 Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). Artery (dpeaa)DE-He213 diaphragm (dpeaa)DE-He213 NADPH oxidase (dpeaa)DE-He213 Kuzmin, Ilya aut Vinogradova, Olga aut Tarasova, Olga aut Enthalten in Artery research Amsterdam : Atlantis Press, 2006 26(2020), Suppl 1 vom: Dez., Seite S50-S50 (DE-627)534057489 (DE-600)2364789-9 1876-4401 nnns volume:26 year:2020 number:Suppl 1 month:12 pages:S50-S50 https://dx.doi.org/10.2991/artres.k.201209.040 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2014 GBV_ILN_2068 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 26 2020 Suppl 1 12 S50-S50 |
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10.2991/artres.k.201209.040 doi (DE-627)SPR054760550 (SPR)artres.k.201209.040-e DE-627 ger DE-627 rakwb eng Borzykh, Anna verfasserin aut P.27 Mechanisms of NADPH Oxidase Participation in the Regulation of Diaphragm Artery Contractile Responses 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Association for Research into Arterial Structure and Physiology 2020 Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). Artery (dpeaa)DE-He213 diaphragm (dpeaa)DE-He213 NADPH oxidase (dpeaa)DE-He213 Kuzmin, Ilya aut Vinogradova, Olga aut Tarasova, Olga aut Enthalten in Artery research Amsterdam : Atlantis Press, 2006 26(2020), Suppl 1 vom: Dez., Seite S50-S50 (DE-627)534057489 (DE-600)2364789-9 1876-4401 nnns volume:26 year:2020 number:Suppl 1 month:12 pages:S50-S50 https://dx.doi.org/10.2991/artres.k.201209.040 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2014 GBV_ILN_2068 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 26 2020 Suppl 1 12 S50-S50 |
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10.2991/artres.k.201209.040 doi (DE-627)SPR054760550 (SPR)artres.k.201209.040-e DE-627 ger DE-627 rakwb eng Borzykh, Anna verfasserin aut P.27 Mechanisms of NADPH Oxidase Participation in the Regulation of Diaphragm Artery Contractile Responses 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Association for Research into Arterial Structure and Physiology 2020 Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). Artery (dpeaa)DE-He213 diaphragm (dpeaa)DE-He213 NADPH oxidase (dpeaa)DE-He213 Kuzmin, Ilya aut Vinogradova, Olga aut Tarasova, Olga aut Enthalten in Artery research Amsterdam : Atlantis Press, 2006 26(2020), Suppl 1 vom: Dez., Seite S50-S50 (DE-627)534057489 (DE-600)2364789-9 1876-4401 nnns volume:26 year:2020 number:Suppl 1 month:12 pages:S50-S50 https://dx.doi.org/10.2991/artres.k.201209.040 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2014 GBV_ILN_2068 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 26 2020 Suppl 1 12 S50-S50 |
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10.2991/artres.k.201209.040 doi (DE-627)SPR054760550 (SPR)artres.k.201209.040-e DE-627 ger DE-627 rakwb eng Borzykh, Anna verfasserin aut P.27 Mechanisms of NADPH Oxidase Participation in the Regulation of Diaphragm Artery Contractile Responses 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Association for Research into Arterial Structure and Physiology 2020 Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). Artery (dpeaa)DE-He213 diaphragm (dpeaa)DE-He213 NADPH oxidase (dpeaa)DE-He213 Kuzmin, Ilya aut Vinogradova, Olga aut Tarasova, Olga aut Enthalten in Artery research Amsterdam : Atlantis Press, 2006 26(2020), Suppl 1 vom: Dez., Seite S50-S50 (DE-627)534057489 (DE-600)2364789-9 1876-4401 nnns volume:26 year:2020 number:Suppl 1 month:12 pages:S50-S50 https://dx.doi.org/10.2991/artres.k.201209.040 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2014 GBV_ILN_2068 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 26 2020 Suppl 1 12 S50-S50 |
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Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. 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p.27 mechanisms of nadph oxidase participation in the regulation of diaphragm artery contractile responses |
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P.27 Mechanisms of NADPH Oxidase Participation in the Regulation of Diaphragm Artery Contractile Responses |
| abstract |
Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). © Association for Research into Arterial Structure and Physiology 2020 |
| abstractGer |
Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). © Association for Research into Arterial Structure and Physiology 2020 |
| abstract_unstemmed |
Reactive oxygen species (ROS) produced by NADPH-oxidase (NOX) participate in vascular tone control, but their effects in the arteries of respiratory muscles is poorly understood. Possible targets of vasoregulatory ROS influence are NO-pathway in the endothelium and Rho-kinase pathway in smooth muscle cells. Therefore, the aim of this study was to evaluate the interaction of NOX-dependent control with NO- and Rho-kinase signaling pathways in rat diaphragm arteries (DA). Methods The segments of DA were isolated from male Wistar rats and mounted in wire myograph (DMT A/S). We studied the effects of NOX inhibitor VAS2870 (1 μM) on contractile responses to a1-adrenergic agonist methoxamine in the absence and in the presence of NO synthase (L-NNA 100 μM) or Rho-kinase (Y27632, 3 μM) inhibitors as well as in the presence of NO donor DEA/NO. Results VAS2879 prominently attenuated the contractile responses of DA to methoxamine (30% decrease of the area under the concentration-response curve). L-NNA and Y27632 increased and decreased methoxamine-induced contraction of DA, respectively. L-NNA did not change the effects of VAS2870 and the sensitivity to DEA/NO did not differ in arteries with active and inhibited NOX. Along with that Y27632 eliminated the effects of VAS2879 on DA contractile responses to methoxamine. Conclusions We showed that NOX-produced ROS potentiate contractile responses of DA. ROS did not affect the activity of NO-pathway in either endothelial or smooth muscle cells of DA. However, ROS modulate the activity of the Rho-kinase pathway in DA smooth muscle cells. Supported by RSF (project No 19-75-00060). © Association for Research into Arterial Structure and Physiology 2020 |
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