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- W2167762007 abstract "Brain-derived natriuretic peptide (BNP) is a cardioprotective peptide released, together with the inactive NH 2 -terminal part of its prohormone (NT-pro-BNP), in response to different kinds of myocardial stress. Hypoglycemia and hypoxemia are conditions that threaten cellular function and hence potentially stimulate BNP release. BNP interacts with the renin-angiotensin system (RAS). The aim of this study was, therefore, to explore if basal RAS activity has an impact on NT-pro-BNP concentrations during myocardial stress induced by hypoglycemia and hypoxemia. From a cohort of 303 healthy young men, 10 subjects with high-RAS activity and 10 subjects with low-RAS activity (age 26 ± 1 yr; mean ± SE) were studied in a single-blinded, randomized, counterbalanced, crossover study on three occasions separated by at least 3 wk: 1) hypoglycemia (mean nadir plasma glucose 2.7 ± 0.5 mmol/l), 2) hypoxemia (mean nadir Po 2 5.8 ± 0.5 kPa), and 3) normoglycemic normoxia (control). NT-pro-BNP was measured at baseline, during the stimuli, and in the recovery phase. Hypoxemia was associated with a 9% increase in NT-pro-BNP from 2.2 ± 1.5 pmol/l at baseline to 2.4 ± 1.5 pmol/l during hypoxemia ( P < 0.001). Hypoglycemia did not affect the NT-pro-BNP level. RAS activity had no impact on NT-pro-BNP levels during hypoglycemia and hypoxemia. Hypoxemia, but not hypoglycemia, stimulates NT-pro-BNP. This indicates that cardiac defense mechanisms against hypoglycemia, if any, are probably different from those against hypoxemia. Basal RAS activity had no impact on NT-pro-BNP levels." @default.
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- W2167762007 date "2008-04-01" @default.
- W2167762007 modified "2023-10-11" @default.
- W2167762007 title "NT-pro-BNP during hypoglycemia and hypoxemia in normal subjects: impact of renin-angiotensin system activity" @default.
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- W2167762007 doi "https://doi.org/10.1152/japplphysiol.01082.2007" @default.
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