Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony

Danilo Fliser, Johannes D Veldhuis, Ralf Dikow, Heinrich Schmidt-Gayk, Eberhard Ritz

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)929-934
Number of pages6
JournalHypertension
Volume32
Issue number5
StatePublished - Nov 1998
Externally publishedYes

Fingerprint

Peptidyl-Dipeptidase A
Aldosterone
Renin
Enalaprilat
Entropy
Hormones
Angiotensins
Angiotensin-Converting Enzyme Inhibitors
Salts

Keywords

  • Aldosterone
  • Angiotensin-converting enzyme inhibitors
  • Entropy
  • Renin
  • Renin- angiotensin-aldosterone system

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Fliser, D., Veldhuis, J. D., Dikow, R., Schmidt-Gayk, H., & Ritz, E. (1998). Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony. Hypertension, 32(5), 929-934.

Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony. / Fliser, Danilo; Veldhuis, Johannes D; Dikow, Ralf; Schmidt-Gayk, Heinrich; Ritz, Eberhard.

In: Hypertension, Vol. 32, No. 5, 11.1998, p. 929-934.

Research output: Contribution to journalArticle

Fliser, D, Veldhuis, JD, Dikow, R, Schmidt-Gayk, H & Ritz, E 1998, 'Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony', Hypertension, vol. 32, no. 5, pp. 929-934.
Fliser D, Veldhuis JD, Dikow R, Schmidt-Gayk H, Ritz E. Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony. Hypertension. 1998 Nov;32(5):929-934.
Fliser, Danilo ; Veldhuis, Johannes D ; Dikow, Ralf ; Schmidt-Gayk, Heinrich ; Ritz, Eberhard. / Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony. In: Hypertension. 1998 ; Vol. 32, No. 5. pp. 929-934.
@article{bc0b85f9237348f0a3965e7e67c96f2b,
title = "Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony",
abstract = "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.",
keywords = "Aldosterone, Angiotensin-converting enzyme inhibitors, Entropy, Renin, Renin- angiotensin-aldosterone system",
author = "Danilo Fliser and Veldhuis, {Johannes D} and Ralf Dikow and Heinrich Schmidt-Gayk and Eberhard Ritz",
year = "1998",
month = "11",
language = "English (US)",
volume = "32",
pages = "929--934",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Effects of acute ACE inhibition on pulsatile renin and aldosterone secretion and their synchrony

AU - Fliser, Danilo

AU - Veldhuis, Johannes D

AU - Dikow, Ralf

AU - Schmidt-Gayk, Heinrich

AU - Ritz, Eberhard

PY - 1998/11

Y1 - 1998/11

N2 - 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.

AB - 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.

KW - Aldosterone

KW - Angiotensin-converting enzyme inhibitors

KW - Entropy

KW - Renin

KW - Renin- angiotensin-aldosterone system

UR - http://www.scopus.com/inward/record.url?scp=0031740026&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031740026&partnerID=8YFLogxK

M3 - Article

C2 - 9822455

AN - SCOPUS:0031740026

VL - 32

SP - 929

EP - 934

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 5

ER -