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NT-pro-BNP during hypoglycemia and hypoxemia in normal subjects: impact of renin-angiotensin system activity

¹Endocrinology Section, Division of Internal Medicine I, Hillerød Hospital, Hillerød; ²Department of Neuroanaesthesia, Neuroscience Centre, Copenhagen University Hospital, Copenhagen; ³Department of Endocrinology, Herlev University Hospital, Herlev, Denmark; and ⁴Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands

Submitted 10 October 2007 ; accepted in final form 5 February 2008

Brain-derived natriuretic peptide (BNP) is a cardioprotective peptide released, together with the inactive NH₂-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 PO₂ 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.

brain-derived natriuretic peptide; angiotensin II; cardiac repolarization

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