Enalapril attenuates natriuresis of atrial natriuretic factor in humans.

Gaillard, C. A.; Koomans, Hein A.; Mees, E. J. Dorhout

doi:10.1161/01.hyp.11.2.160

Cited by 34 publications

(24 citation statements)

References 31 publications

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“…Despite this close relationship, few studies have been reported in the literature on the effects of blockade of the renin-angiotensin-aldosterone system by converting enzyme inhibitors on the pharmacological actions or plasma levels of ANP. It has been shown in Wistar rats that the natriuretic action of infusion of ANP is not influenced by pretreatment with captopril (Hirata et al, 1987). Data on the influence of converting enzyme inhibition on the hypotensive effect of an ANP infusion are inconsistent since both a potentiation (Awah et al, 1986) and no effect (Hirata et al, 1987;Hansell & Ulfendahl, 1987;Gaillard et al, 1988) have been reported. Finally, it has recently been shown in humans that the vasodilatory effect of an intra-arterial infusion of ANP is not influenced by pretreatment with captopril (Hughes et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

The effect of acute ACE inhibition on atrial natriuretic peptide.

Doorenbos

Brummelen

1989

Brit J Clinical Pharma

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1 The effect of acute angiotensin converting enzyme (ACE) inhibition on the plasma concentrations of atrial natriuretic peptide (ANP) was investigated in a single-blind placebo controlled crossover study in healthy volunteers. 2 Intravenous infusion of 2 mg cilazaprilat resulted in a significant and short lasting inhibition of ACE as evidenced by a decrease of plasma angiotensin II and an increase in plasma renin activity. 3 When compared with placebo cilazaprilat lowered diastolic pressure and increased heart rate significantly. 4 No effect of cilazaprilat was found on plasma ANP levels, suggesting that angiotensin II does not mediate ANP release.

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Section: Introductionmentioning

confidence: 99%

The effect of acute ACE inhibition on atrial natriuretic peptide.

Doorenbos

Brummelen

1989

Brit J Clinical Pharma

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“…Remarkably, the magnitude of this attenuation was comparable with that seen in our previous study, where the subjects consumed only 100 mmol sodium daily. 5 Apparently, a 300 mmol sodium diet, as supplied in the present study, does not suppress the renal renin-angiotensin system to the extent of eliminating the effects of converting enzyme inhibition on the kidney. The data on lithium, free water clearance, and excretion of other electrolytes are compatible with less suppression by ANF of (fractional) tubular solute reabsorption at proximal and distal nephron segments during converting enzyme inhibition than before converting enzyme inhibition.…”

Section: Discussionmentioning

confidence: 55%

Opposite effects of enalapril and nitrendipine on natriuretic response to atrial natriuretic factor. Renal function evaluated with clearance studies in humans.

Gaillard¹,

Koomans²,

Rabelink³

et al. 1989

Hypertension

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In clearance studies, we analyzed the effect of Ca }+ entry blockade with nitrendipine treatment (20 mg b.i.d. for 4 days) and of converting enzyme inhibition with enalapril treatment (20 mg b.i.d. for 4 days) on renal response to atrial natriuretic factor (ANF) (25 fig bolus followed by an infusion of 0.03 /tg/kg/min for 90 minutes) in six healthy volunteers who were taking 300 mmol sodium daily. In a control study ANF was administered without Ca 2+ entry blockade or converting enzyme inhibition. Natriuresis rose from 239±38 to 605±137 /imol/min in the control study (p<0.05), from 330±53 to 943±152 /unol/min with Ca 2+ entry blockade (p<0.05), and from 236±22 to 344±39 /unol/min with converting enzyme inhibition (NS). ANF induced a rise in mairinial free water clearance, inulin clearance, and in the excretion of multiple electrolytes except potassium. Fractional lithium reabsorption fell. In general, these effects were stronger during Ca 2+ entry blockade and blunted during converting enzyme inhibition. p-Aminohippurate clearance tended to decrease during the control study (NS), remained constant during Ca 2+ entry blockade, and decreased significantly when ANF was infused during converting enzyme inhibition (p<0.05 vs. control and vs. Ca 2+ entry blockade study). Blood pressure was lowered by Ca 2+ entry blockade and, to a somewhat greater extent, by converting enzyme inhibition, but ANF administration induced no additional fall except for a short-term drop during Ca I+ entry blockade. From these data we conclude that, in healthy humans, the effects of ANF on natriuresis and renal sodium handling are enhanced by Ca 2+ entry blockade and blunted by converting enzyme inhibition. These effects might be explained by amplification of (preglomerular?) ANF-induced vasodilation during Ca 2+ entry blockade and amplification of (postglomerular?) ANF-induced vasoconstriction during converting enzyme inhibition. {Hypertension 1989;13:173-180) I n isolated perfused rat kidneys Ca 2+ entry blockade with verapamil was reported to inhibit the hemodynamic and natriuretic effect of atrial extract.1 By contrast, it was recently shown that nifedipine, although preventing the renal hemodynamic effect, potentiated the natriuretic effect of atrial natriuretic factor (ANF) in anesthetized rabbits.2 This study 2 could not confirm inhibition of ANF-natriuresis, but it was considered that anes- thesia and subsequent decreased renal nerve activity might have caused this new finding. Data in conscious animals or in humans are not available. Since Ca 2+ entry blockade interferes with the action of neurohumoral mechanisms such as renal sympathetic nerve activity and the renin-angiotensin system, 3 one way in which Ca 2+ entry blockade could influence the effect of ANF is by attenuating the effect of endogenous angiotensin II on the kidney. It was found by others 4 and by us 5 that angiotensin I converting enzyme inhibition blunts the natriuretic effect of ANF in humans. Although the mechanism of this interaction is not clear, it can be hypo...

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“…Wilkins et al 12 employed short-term (15 minutes), high-dose infusions of ANF and reported a nonsignificant trend toward higher intrainfusion plasma ANF values. Gaillard et al 14 gave bolus injections of ANF (100 ^g) and reported a similar, slight, and statistically insignificant trend toward higher peak ANF values after enalapril. We chose a dose (1.5 pmol/kg/min) and duration (3 hours) of ANF that induced plasma ANF concentrations within the lower part of the clinical pathophysiological range, 2223 which allowed steady-state values of plasma ANF to be established, and which is known to exert biological effects, 24 -26 including natriuresis.…”

Section: Discussionmentioning

confidence: 77%

“…Gaillard et al 14 documented a shift in baseline PAH clearance between study days, further adding to difficulty in interpretation of data from that study.…”

Section: Ns Nsmentioning

confidence: 91%

Interaction of angiotensin converting enzyme inhibition and atrial natriuretic factor.

et al. 1989

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The interaction of angiotensin converting enzyme (ACE) inhibition and atrial natriuretic factor (ANF) was investigated in six supine, sodium-replete, normal volunteers who received captopril (10 mg i.v. bolus followed by 10 mg/hr constant infusion) or vehicle superimposed on background 3-hour, constant, low-dose (1.5 pmol/kg/min) infusions of human ANF (99-126). Plasma converting enzyme activity was significantly inhibited but this had no effect on endogenous plasma ANF concentrations. ANF infusions, with or without captopril, caused similar increases in plasma ANF concentrations, and calculated metabolic clearance rates for ANF were unchanged. Similarly, blood pressure, heart rate, renal blood flow, glomerular filtration rate, and renal electrolyte excretion, including ANF-induced natriuresis, were unaffected by captopril. The combination of ANF plus captopril produced a significant increase in plasma aldosterone (79±8 vs. 60±6 pmol/1, p<0.05), cortisol (406±52 vs. 265±29 nmol/1, /><0.01), adrenaline (119±21 vs. 76±10 pg/ml, p<0.05), and noradrenaline (319±49 vs. 215±38 pg/ml, p<0.05) compared with tune-matched placebo data. Converting enzyme inhibition, in the absence of major changes in blood pressure or renal blood flow, has little effect on ANF metabolism or renal bioactivity. However, ACE inhibition and ANF combined may interact to increase activity of the hypothalamo-pituitary-adrenai axis and sympathetic nervous system by unknown mechanisms. (Hypertension 1989; 13:193-199) A trial natriuretic factor (ANF) with its diverse actions on renal and hemodynamic function and vasoactive hormone activity 1 continues to attract attention as a potentially major regulator of body fluid volume and arterial pressure. In many tissues ANF and the renin-angiotensin system appear to be counterbalanced.2 Angiotensin converting enzyme (ACE) inhibitors are now employed with increasing frequency in the treatment of both hypertension and heart failure. Recent trials demonstrate that ACE inhibitors improve survival in heart failure 3 and preserve renal function in diabetic patients. 4 Further major expansion in the use of these agents is likely. For these reasons, study of any possible interaction between ANF and ACE activity is relevant to the physiology of sodium balance and may have important clinical consequences.Already there is a body of circumstantial evidence pointing to an interaction between ACE inhibition

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Enalapril attenuates natriuresis of atrial natriuretic factor in humans.

Cited by 34 publications

References 31 publications

The effect of acute ACE inhibition on atrial natriuretic peptide.

The effect of acute ACE inhibition on atrial natriuretic peptide.

Opposite effects of enalapril and nitrendipine on natriuretic response to atrial natriuretic factor. Renal function evaluated with clearance studies in humans.

Interaction of angiotensin converting enzyme inhibition and atrial natriuretic factor.

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