title: NT-pro-BNP during hypoglycemia and hypoxemia in normal subjects: impact of renin-angiotensin system activity.
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.
authors.affiliation: Endocrinology Section, Division of Internal Medicine I, Hillerød Hospital, Helsevej 2, DK-3400 Hillerød, Denmark. rsa@noh.regionh.dk
authors.forename: R
authors.initials: R
authors.lastname: Due-Andersen
authors.forename: U
authors.initials: U
authors.lastname: Pedersen-Bjergaard
authors.forename: T
authors.initials: T
authors.lastname: Høi-Hansen
authors.forename: N V
authors.initials: NV
authors.lastname: Olsen
authors.forename: C
authors.initials: C
authors.lastname: Kistorp
authors.forename: J
authors.initials: J
authors.lastname: Faber
authors.forename: F
authors.initials: F
authors.lastname: Boomsma
authors.forename: B
authors.initials: B
authors.lastname: Thorsteinsson
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D018592:Cross-Over Studies; D006801:Humans; D007003:Hypoglycemia / Q000139:chemically induced / Q000378:metabolism*; D007004:Hypoglycemic Agents; D000860:Hypoxia / Q000378:metabolism*; D007328:Insulin; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000378:metabolism*; D010446:Peptide Fragments / Q000378:metabolism*; D012016:Reference Values; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D000804:Angiotensin II; D020097:Natriuretic Peptide, Brain; D012083:Renin