Key result
Acute ACE inhibition with enalaprilat significantly increased 24-hour pulsatile and total renin secretion (P<0.01) without affecting basal or pulsatile aldosterone secretion.
Why the study?
Does acute enalaprilat administration alter the pattern of renin and aldosterone secretion in healthy men?
RCT (n=8)
random order
Does acute enalaprilat administration alter the pattern of renin and aldosterone secretion in healthy men?
Acute ACE inhibition increases pulsatile renin secretion without affecting aldosterone secretion, suggesting the renin-angiotensin-aldosterone axis may not be completely uncoupled by acute ACE inhibition or is driven by a common signal generator.
Answers are grounded in this paper and cite their sources.
Acute ACE inhibition spares aldosterone secretion despite boosting pulsatile renin; extends RAAS pulsatility models in healthy volunteers.
Pulsatile (burstlike) secretion of renin and aldosterone is positively coupled with a short time lag of about 10 to 20 minutes. We investigated how acute interruption of the renin-angiotensin-aldosterone axis, ie, acute angiotensin-converting enzyme (ACE) inhibition, alters the pattern of renin and aldosterone secretion. Eight healthy men (mean age, 22+/-1 years) were studied while on standardized salt intake. They were allocated on 2 occasions in random order to injection of placebo or 1.25 mg of the ACE inhibitor enalaprilat. Blood samples were obtained every 10 minutes for 24 hours for measurement of plasma renin and aldosterone concentrations. The hormone concentration profiles were analyzed using a multiparameter deconvolution technique; basal (tonic) and pulsatile hormone secretion was assessed. The regularity of pulsatile hormone secretion was analyzed using approximate entropy (ApEn). Cross-correlation and cross-ApEn analysis of renin and aldosterone secretion were performed to assess synchrony. Acute ACE inhibition caused an immediate burst of renin release and, in addition, significantly (P<0.01) increased 24-hour pulsatile and total renin secretion. It did not affect basal (nonpulsatile) renin secretion. The amplitude of renin bursts and the mass of hormone secreted per burst were significantly (P<0.01) increased, whereas the burst frequency (ie, number of secretory events) was unchanged. ApEn analysis revealed significantly (P<0.05) more regular renin secretion after ACE inhibition. In contrast, neither basal nor pulsatile aldosterone secretion was affected by administration of enalaprilat. Cross-ApEn analysis documented not only a maintained pattern of reproducibility (ie, synchrony) but also greater conditional regularity between pulsatile renin and aldosterone secretions with acute ACE inhibition. However, the quantitative strength of hormone coupling (assessed by cross-correlation analysis) was markedly diminished by enalaprilat treatment. The present findings suggest that the renin-angiotensin-aldosterone axis may not be completely uncoupled by acute ACE inhibition or that pulsatile renin and aldosterone secretion is driven by a common signal generator that is unaffected by ACE inhibition. In addition, a background basal and pulsatile aldosterone secretion not regulated by the renin-angiotensin axis may exist.
No takes yet. Share an insight, caveat, or question.
Fliser et al. (1998) conducted an RCT in Healthy (n=8). Enalaprilat vs. Placebo was evaluated on 24-hour pulsatile and total renin secretion (p=<0.01). Acute ACE inhibition with enalaprilat significantly increased 24-hour pulsatile and total renin secretion (P<0.01) without affecting basal or pulsatile aldosterone secretion.
Synapse has enriched 10 related papers. Consider them for comparative context: