Brain natriuretic peptide and acute hypobaric hypoxia in humans

Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evi...
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Autor*in:	Woods, David [verfasserIn] Hooper, Tim Mellor, Adrian Hodkinson, Pete Wakeford, Rob Peaston, Bob Ball, Steve Green, Nic

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2011

Schlagwörter:	Hypobaric hypoxia Brain natriuretic peptide Altitude

Anmerkung:	© The Physiological Society of Japan and Springer 2011

Übergeordnetes Werk:	Enthalten in: The journal of physiological sciences - [Tokyo] : Springer, 2006, 61(2011), 3 vom: 24. März, Seite 217-220
Übergeordnetes Werk:	volume:61 ; year:2011 ; number:3 ; day:24 ; month:03 ; pages:217-220

Links:	Volltext

DOI / URN:	10.1007/s12576-011-0141-3

Katalog-ID:	SPR026166186

Internformat


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100	1		\|a Woods, David \|e verfasserin \|4 aut
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520			\|a Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion.
650		4	\|a Hypobaric hypoxia \|7 (dpeaa)DE-He213
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allfields	10.1007/s12576-011-0141-3 doi (DE-627)SPR026166186 (SPR)s12576-011-0141-3-e DE-627 ger DE-627 rakwb eng Woods, David verfasserin aut Brain natriuretic peptide and acute hypobaric hypoxia in humans 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer 2011 Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. Hypobaric hypoxia (dpeaa)DE-He213 Brain natriuretic peptide (dpeaa)DE-He213 Altitude (dpeaa)DE-He213 Hooper, Tim aut Mellor, Adrian aut Hodkinson, Pete aut Wakeford, Rob aut Peaston, Bob aut Ball, Steve aut Green, Nic aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 61(2011), 3 vom: 24. März, Seite 217-220 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:61 year:2011 number:3 day:24 month:03 pages:217-220 https://dx.doi.org/10.1007/s12576-011-0141-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 61 2011 3 24 03 217-220
spelling	10.1007/s12576-011-0141-3 doi (DE-627)SPR026166186 (SPR)s12576-011-0141-3-e DE-627 ger DE-627 rakwb eng Woods, David verfasserin aut Brain natriuretic peptide and acute hypobaric hypoxia in humans 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer 2011 Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. Hypobaric hypoxia (dpeaa)DE-He213 Brain natriuretic peptide (dpeaa)DE-He213 Altitude (dpeaa)DE-He213 Hooper, Tim aut Mellor, Adrian aut Hodkinson, Pete aut Wakeford, Rob aut Peaston, Bob aut Ball, Steve aut Green, Nic aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 61(2011), 3 vom: 24. März, Seite 217-220 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:61 year:2011 number:3 day:24 month:03 pages:217-220 https://dx.doi.org/10.1007/s12576-011-0141-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 61 2011 3 24 03 217-220
allfields_unstemmed	10.1007/s12576-011-0141-3 doi (DE-627)SPR026166186 (SPR)s12576-011-0141-3-e DE-627 ger DE-627 rakwb eng Woods, David verfasserin aut Brain natriuretic peptide and acute hypobaric hypoxia in humans 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer 2011 Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. Hypobaric hypoxia (dpeaa)DE-He213 Brain natriuretic peptide (dpeaa)DE-He213 Altitude (dpeaa)DE-He213 Hooper, Tim aut Mellor, Adrian aut Hodkinson, Pete aut Wakeford, Rob aut Peaston, Bob aut Ball, Steve aut Green, Nic aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 61(2011), 3 vom: 24. März, Seite 217-220 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:61 year:2011 number:3 day:24 month:03 pages:217-220 https://dx.doi.org/10.1007/s12576-011-0141-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 61 2011 3 24 03 217-220
allfieldsGer	10.1007/s12576-011-0141-3 doi (DE-627)SPR026166186 (SPR)s12576-011-0141-3-e DE-627 ger DE-627 rakwb eng Woods, David verfasserin aut Brain natriuretic peptide and acute hypobaric hypoxia in humans 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer 2011 Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. Hypobaric hypoxia (dpeaa)DE-He213 Brain natriuretic peptide (dpeaa)DE-He213 Altitude (dpeaa)DE-He213 Hooper, Tim aut Mellor, Adrian aut Hodkinson, Pete aut Wakeford, Rob aut Peaston, Bob aut Ball, Steve aut Green, Nic aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 61(2011), 3 vom: 24. März, Seite 217-220 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:61 year:2011 number:3 day:24 month:03 pages:217-220 https://dx.doi.org/10.1007/s12576-011-0141-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 61 2011 3 24 03 217-220
allfieldsSound	10.1007/s12576-011-0141-3 doi (DE-627)SPR026166186 (SPR)s12576-011-0141-3-e DE-627 ger DE-627 rakwb eng Woods, David verfasserin aut Brain natriuretic peptide and acute hypobaric hypoxia in humans 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer 2011 Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. Hypobaric hypoxia (dpeaa)DE-He213 Brain natriuretic peptide (dpeaa)DE-He213 Altitude (dpeaa)DE-He213 Hooper, Tim aut Mellor, Adrian aut Hodkinson, Pete aut Wakeford, Rob aut Peaston, Bob aut Ball, Steve aut Green, Nic aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 61(2011), 3 vom: 24. März, Seite 217-220 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:61 year:2011 number:3 day:24 month:03 pages:217-220 https://dx.doi.org/10.1007/s12576-011-0141-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 61 2011 3 24 03 217-220
language	English
source	Enthalten in The journal of physiological sciences 61(2011), 3 vom: 24. März, Seite 217-220 volume:61 year:2011 number:3 day:24 month:03 pages:217-220
sourceStr	Enthalten in The journal of physiological sciences 61(2011), 3 vom: 24. März, Seite 217-220 volume:61 year:2011 number:3 day:24 month:03 pages:217-220
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Hypobaric hypoxia Brain natriuretic peptide Altitude
isfreeaccess_bool	false
container_title	The journal of physiological sciences
authorswithroles_txt_mv	Woods, David @@aut@@ Hooper, Tim @@aut@@ Mellor, Adrian @@aut@@ Hodkinson, Pete @@aut@@ Wakeford, Rob @@aut@@ Peaston, Bob @@aut@@ Ball, Steve @@aut@@ Green, Nic @@aut@@
publishDateDaySort_date	2011-03-24T00:00:00Z
hierarchy_top_id	572081235
id	SPR026166186
language_de	englisch
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spellingShingle	Woods, David misc Hypobaric hypoxia misc Brain natriuretic peptide misc Altitude Brain natriuretic peptide and acute hypobaric hypoxia in humans
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topic_title	Brain natriuretic peptide and acute hypobaric hypoxia in humans Hypobaric hypoxia (dpeaa)DE-He213 Brain natriuretic peptide (dpeaa)DE-He213 Altitude (dpeaa)DE-He213
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title	Brain natriuretic peptide and acute hypobaric hypoxia in humans
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title_full	Brain natriuretic peptide and acute hypobaric hypoxia in humans
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title_sort	brain natriuretic peptide and acute hypobaric hypoxia in humans
title_auth	Brain natriuretic peptide and acute hypobaric hypoxia in humans
abstract	Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. © The Physiological Society of Japan and Springer 2011
abstractGer	Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. © The Physiological Society of Japan and Springer 2011
abstract_unstemmed	Abstract In animal models, the secretion of the cardiac hormone, brain natriuretic peptide (BNP), and its closely related peptide, atrial natriuretic peptide (ANP), are stimulated by acute hypoxia. There is extensive human evidence for a rise in ANP under acute hypoxic conditions but very little evidence regarding the BNP response to acute hypoxia in humans. We therefore subjected seven healthy subjects to an acute hypobaric hypoxic stimulus to examine if BNP secretion increases rapidly. Significant hypoxaemia (mean nadir oxygen saturation 62.3%) was induced but no significant rise in BNP occurred. This suggests that either such acute hypoxaemia is well tolerated by the healthy human heart or it is not a stimulus for BNP secretion. © The Physiological Society of Japan and Springer 2011
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title_short	Brain natriuretic peptide and acute hypobaric hypoxia in humans
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Brain natriuretic peptide and acute hypobaric hypoxia in humans

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