The effect of acute ACE inhibition on atrial natriuretic peptide.

Doorenbos, C. J.; Brummelen, P. Van

doi:10.1111/j.1365-2125.1989.tb03488.x

Cited by 12 publications

(2 citation statements)

References 16 publications

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“…The authors of this study [17] conclude that the natriuretic effect of ACE inhibitors may be caused by change during ACE inhibition. This is in accordance with other studies [14,15]. their antihypertensive action.…”

Section: Posm Values the Reason For The Discrepancy Betweensupporting

confidence: 94%

Short-term ACE inhibition has no effect on sodium and water excretion during PEEP ventilation

Wenz

Eckelt

Rissel

et al. 1997

EJA

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The short-term effect of intravenous (i.v.) angiotensin converting enzyme (ACE) inhibitor enalaprilat in 10 critically ill patients, being ventilated with positive end-expiratory pressure (PEEP), on sodium and water excretion was investigated. Mean arterial pressure (MAP) decreased. Heart rate and central venous pressure (CVP) did not change. Glomerular filtration rate (GFR), urine volume (V) and sodium excretion (UNaV) decreased in two patients with reduced MAP. GFR, V and UNaV increased in two patients with decreased MAP. No relation between changes in MAP and excretion was observed in six patients. ACE decreased in all patients. Plasma renin activity increased, aldosterone decreased, while atrial natriuretic peptide as well as antidiuretic hormone did not change. Enalaprilat did not facilitate sodium and water excretion during ventilation with PEEP. Decreased MAP indicates that the investigated patients were very dependent on their renin-angiotensin system to maintain systemic perfusion pressure. Base-line MAP and CVP values were no predictors of haemodynamic and excretory changes following acute ACE inhibition.

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Section: Posm Values the Reason For The Discrepancy Betweensupporting

confidence: 94%

Short-term ACE inhibition has no effect on sodium and water excretion during PEEP ventilation

Wenz

Eckelt

Rissel

et al. 1997

EJA

View full text Add to dashboard Cite

show abstract

“…This is in agreement with other published reports. 23,59,60 Intra-arterial thiorphan did not produce a detectable increase in ANP concentrations in venous blood draining the infused arm. However, any changes in local ANP concentrations are likely to be small and may have been below the sensitivity of the assay.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Neutral Endopeptidase Causes Vasoconstriction of Human Resistance Vessels In Vivo

et al. 1998

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Background-Neutral endopeptidase (NEP) degrades vasoactive peptides, including the natriuretic peptides, angiotensin II, and endothelin-1. Systemic inhibition of NEP does not consistently lower blood pressure, even though it increases natriuretic peptide concentrations and causes natriuresis and diuresis. We therefore investigated the direct effects of local inhibition of NEP on forearm resistance vessel tone. Methods and Results-Four separate studies were performed, each with 90-minute drug infusions. In the first study, 10 healthy subjects received a brachial artery infusion of the NEP inhibitor candoxatrilat (125 nmol/min), which caused a slowly progressive forearm vasoconstriction (12Ϯ2%; Pϭ0.001). In a second two-phase study, 6 healthy subjects received, 4 hours after enalapril (20 mg) or placebo, an intra-arterial infusion of the NEP inhibitor thiorphan (30 nmol/min). Thiorphan caused similar degrees of local forearm vasoconstriction (Pϭ0.6) after pretreatment with both placebo (13Ϯ1%, Pϭ0.006) and enalapril (17Ϯ6%, Pϭ0.05). In a third three-phase study, 8 healthy subjects received intra-arterial thiorphan (30 nmol/min), the endothelin ET A antagonist BQ-123 (100 nmol/min), and both combined.

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Effects of Ketanserin on Lipids, Lipoproteins, and Plasma Atrial Natriuretic Factor in Patients with Essential Hypertension

Bielmann

Leduc

Gutkowska

et al. 1990

The Journal of Clinical Pharma

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The effects of ketanserin, 40 mg/day (KE40) and 80 mg/day (KE80) on mean arterial pressure, lipids, lipoproteins, and circulating atrial natriuretic factor (ANF) were investigated in a 24-week controlled study in 29 patients suffering from mild to moderate hypertension. A significant decrease in mean arterial pressure (MAP) was observed after 18 weeks of therapy, accompanied by a 64% (P less than .05) and 80% (P less than .02) increase in circulating ANF levels with KE40 and KE80, respectively. There were no significant changes in mean total cholesterol, triglycerides, or cholesterol of the high density lipoproteins (HDL), low density lipoproteins (LDL), and very low density lipoproteins (VLDL) fractions. There was a significant increase in the mean apo B levels and consequently a slight but statistically significant decrease in the ratio of LDL C/B. It is concluded that both doses of KE are effective for monotherapy of mild to moderate essential hypertension. The drug sharply increases circulating ANF levels without significantly altering the plasma lipids. In contrast, by increasing the apolipoprotein B content of the LDL fraction, the beneficial cardiovascular effect of a lowered blood pressure may be partly blunted.

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The effect of acute ACE inhibition on atrial natriuretic peptide.

Cited by 12 publications

References 16 publications

Short-term ACE inhibition has no effect on sodium and water excretion during PEEP ventilation

Short-term ACE inhibition has no effect on sodium and water excretion during PEEP ventilation

Inhibition of Neutral Endopeptidase Causes Vasoconstriction of Human Resistance Vessels In Vivo

Effects of Ketanserin on Lipids, Lipoproteins, and Plasma Atrial Natriuretic Factor in Patients with Essential Hypertension

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