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

Gaillard, C. A.; Koomans, Hein A.; Rabelink, Ton J.; Boer, P. de; Mees, E. J. Dorhout

doi:10.1161/01.hyp.13.2.173

Cited by 6 publications

(1 citation statement)

References 32 publications

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“…Strikingly, in their and our studies enhancement of ANF natriuresis occurred despite a lower arterial pressure during nitrendipine. Because we found that the rise in GFR after ANF was also amplified during nitrendipine (Gaillard et al 1989), the enhanced natriuretic effect may very well concern potentiation by calcium entry blockade of the vascular effects of ANF. This is conceivable, since both calcium entry blockade as ANF cause relaxation of afferent arterioles, the mesangium, and the medullary vasculature, and reset tubulo-glomerular feedback (Bell 1987;Zeidel and Brenner 1987).…”

Section: Different Effect In Hypertensivesmentioning

confidence: 86%

The Diuretic Effect of Calcium Entry Blockade in Normals and Hypertensive Patients.

Geyskes¹,

Schaik²,

Gaillard³

et al. 1992

Tohoku J. Exp. Med.

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Calcium entry blockers have been shown to exert hemodynamic and diuretic effects in the kidney. The diuretic effects can be demonstrated most clearly in the isolated perfused kidney, not influenced by compensatory mechanisms such as a lower blood pressure or changes of hormones. However, they can also be shown in vivo in humans. We studied the renal effects of calcium entry blockade after the first dosage and after continued oral dosages of 20 mg nicardipine tid in patients with essential hypertension and in normotensive controls. Renal function was determined during maximal free water clearance, allowing estimation of changes in "proximal" and "distal" tubular sodium reabsorption . Results showed a natriuretic effect. In the control subjects, clearance results were compatible with a decrease of proximal and distal tubular reabsorption, but in the hypertensive group natriuresis was mainly achieved by an increase of the glomerular filtration rate and a decrease of fractional distal reabsorption. In both groups the natriuresis occurred concomitantly with a lower blood pressure. The ratio plasma renin activity/plasma aldosterone concentration increased, although nicardipine did not inhibit the increase of plasma aldosterone during angiotensin II infusion. Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Facilitation of sodium excretion by human ANF may be an additional diuretic mechanism of calcium entry blockers.atrial natriuretic factor ; calcium entry blockade ; diuretic ; nicardipine ; sodium excretion Calcium entry blockade has been shown to exert diuretic effects. This occurs in the perfused kidney, isolated from influences of hormones and changes of arterial pressure, as well as in vivo in experimental mammals and man (Luft 1987). Despite abundant experimental demonstration of this effect, no single or principal mechanism has as yet been demonstrated. Evidence has indeed accumulated that the sodium and water excretion during calcium entry blockade has multiple causes, which even may vary among the many drugs of this class. For instance, only verapamil and diltiazem have been shown to decrease the short

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Section: Different Effect In Hypertensivesmentioning

confidence: 86%

The Diuretic Effect of Calcium Entry Blockade in Normals and Hypertensive Patients.

Geyskes¹,

Schaik²,

Gaillard³

et al. 1992

Tohoku J. Exp. Med.

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Natriuretic Peptides and Normal Body Fluid Regulation

Bie

2018

Comprehensive Physiology

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Natriuretic peptides are structurally related, functionally diverse hormones. Circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are delivered predominantly by the heart. Two C-type natriuretic peptides (CNPs) are paracrine messengers, notably in bone, brain, and vessels. Natriuretic peptides act by binding to the extracellular domains of three receptors, NPR-A, NPR-B, and NPR-C of which the first two are guanylate cyclases. NPR-C is coupled to inhibitory proteins. Atrial wall stress is the major regulator of ANP secretion; however, atrial pressure changes plasma ANP only modestly and transiently, and the relation between plasma ANP and atrial wall tension (or extracellular volume or sodium intake) is weak. Absence and overexpression of ANP-related genes are associated with modest blood pressure changes. ANP augments vascular permeability and reduces vascular contractility, renin and aldosterone secretion, sympathetic nerve activity, and renal tubular sodium transport. Within the physiological range of plasma ANP, the responses to step-up changes are unimpressive; in man, the systemic physiological effects include diminution of renin secretion, aldosterone secretion, and cardiac preload. For BNP, the available evidence does not show that cardiac release to the blood is related to sodium homeostasis or body fluid control. CNPs are not circulating hormones, but primarily paracrine messengers important to ossification, nervous system development, and endothelial function. Normally, natriuretic peptides are not powerful natriuretic/diuretic hormones; common conclusions are not consistently supported by hard data. ANP may provide fine-tuning of reno-cardiovascular relationships, but seems, together with BNP, primarily involved in the regulation of cardiac performance and remodeling. © 2017 American Physiological Society. Compr Physiol 8:1211-1249, 2018.

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Krekels

Gaillard

Viergever

et al. 1997

Cardiovascular Drugs and Therapy

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This study investigated whether the acute natriuretic effect of nitrendipine is related to its initial renal hemodynamic effects. We investigated 16 patients (10 men and 6 women, mean age 52 +/- 2 years) with essential hypertension, whose treatment, if any, was stopped 3 weeks before the study. They were admitted to a metabolic ward for 9 days and kept on a constant sodium diet of 55 mmol/day. During two 24-hour experiments, subjects randomly received a single oral dose of placebo/nitrendipine 10 mg (group 1, n = 8) or placebo/nitrendipine 20 mg (group 2, n = 8), according to a double-blind crossover study design. Patients fasted during the experiments, but their sodium intake was ensured by a constant intravenous saline infusion of 2.3 mmol/hr. Mean arterial pressure (MAP) and heart rate were determined for 5 hours following the administration of nitrendipine or placebo. Effective renal plasma flow (ERPF), glomerular filtration rate, active plasma renin concentration, angiotensin II, aldosterone, atrial natriuretic peptide, and catecholamines were determined every hour for 5 hours. Hourly urine collections were used to assess sodium, potassium, and creatinine excretions. Relative to placebo, only in group 2 (nitrendipine 20 mg) was a fall in MAP and a rise in ERPF observed 2 hours after the start of the experiment. The effects, however, lasted only for 1 hour. No such changes were seen in group 1. In neither group did nitrendipine affect hormonal concentrations. Sodium excretion was enhanced after the 20-mg dose of nitrendipine only (p < 0.05). Nitrendipine 20 mg induced a significant increase in sodium excretion, which may be dissociated from its acute hemodynamic effects.

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

Cited by 6 publications

References 32 publications

The Diuretic Effect of Calcium Entry Blockade in Normals and Hypertensive Patients.

The Diuretic Effect of Calcium Entry Blockade in Normals and Hypertensive Patients.

Natriuretic Peptides and Normal Body Fluid Regulation

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