Effects of Verapamil and Nifedipine on Renal Function and Hemodynamics in the Dog

Bell, Anthony J.; Lindner, A

doi:10.1159/000172955

Cited by 39 publications

(32 citation statements)

References 26 publications

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“…In one of these studies, 49 the increments in RBF, GFR, and U Nl were similar to those in the aforementioned studies in which blood pressure remained constant. However, in the two other studies, 3254 the decrease in systemic blood pressure was accompanied by natriuresis but no significant changes in RBF or GFR.…”

Section: Effects Of Calcium Blockers On Renal Hemodynamics and Renal supporting

confidence: 76%

Multiple effects of calcium entry blockers on renal function in hypertension.

Romero

Raij²,

Granger

et al. 1987

Hypertension

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SUMMARY Characterization of the renal effects of calcium entry blockers has not been easy because the inhibition of Ca 2+ cellular influx alters several regulatory functions. The ability of calcium blockers to dilate renal vasculature and to increase glomerular filtration rate is largely determined by the preexisting vascular tone. However, the increments in sodium excretion could occur without alterations in renal hemodynamics. Calcium blockers could increase sodium excretion by inducing a redistribution of renal blood flow toward juxtamedullary nephrons, by inhibiting tubuloglomerular feedback responses, or by a direct action on the tubular transport of sodium. These effects are poorly understood at present. In vitro studies show that the blockade of calcium entry enhances renin secretion and decreases prostaglandin synthesis. This dissociation has not been found during longterm administration, which has been proved to be effective for the treatment of essential hypertension with normal maintenance of renal function. In this respect, there are reports indicating that calcium blockers are particularly effective in a subgroup of patients with essential hypertension who exhibit subtle but detectable alterations in calcium metabolism. Further studies are needed to determine whether this significant response to calcium blockers is due to correction of an early defect of calcium cellular kinetics that initiated the increase in blood pressure. (Hypertension 10: 140-151, 1987) KEY WORDS • glomerular filtration rate blood flow • glomerular mesangium renin-angiotensin-prostaglandin system * renal C ALCIUM entry blockers are relatively new drugs that are gaining rapid acceptance for the treatment of hypertension. '" 3 In fact, their potent properties for relaxing smooth muscle 4 could well account for their efficacy in lowering the increase of total peripheral resistance in patients with hypertension. 5 However, a fundamental concept implicit in the evaluation of any antihypertensive drug is related to its effect on renal function 6 because a decrease in renal perfusion pressure induces several compensatory reac-

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Section: Effects Of Calcium Blockers On Renal Hemodynamics and Renal supporting

confidence: 76%

Multiple effects of calcium entry blockers on renal function in hypertension.

Romero

Raij²,

Granger

et al. 1987

Hypertension

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“…Ichikawa et al (4) found that verapamil markedly inhibits the ANG II-induced de creases in glomerular plasma flow and filtra tion coefficient. Nifedipine was reported to suppress the decreasing action of ANG II on renal blood flow (RBF) (5,6). Similar results were observed with other calcium channel blockers, such as diltiazem (7) and nitrendi pine (8).…”

Section: Nisoldipinesupporting

confidence: 60%

Inhibitory effects of nisoldipine and saralasin on angiotensin II-induced antidiuresis in anesthetized dogs.

et al. 1990

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Abstract-Inhibitory effects of the calcium channel blocker nisoldipine on angio tensin II-induced antidiuresis were investigated in anesthetized dogs, and the findings were compared with those of saralasin.Intrarenal arterial infusion of 10 ng/kg/min angiotensin II resulted in marked decreases in renal blood flow (RBF) and urine formation, with a relatively moderate decrease in glomerular filtration rate. There were marked reductions in the fractional excretion of lithium, which is used as an index of the fractional proximal excretion of sodium, and the fractional distal excretion of sodium.Nisoldipine (50 ng/kg/min) administered intrarenally produced a partial inhibition on the decreased response of RBF to angiotensin II. The peptide-induced decreases in urine flow, urinary excretion of electrolytes and fractional excretion of electrolytes were abolished by nisoldipine. In contrast, when saralasin was administered intrarenally at 10 ng/kg/min, a dose which could partially inhibit the angiotensin 11-induced decrease in RBF to the same extent as seen with nisoldipine, the antagonist attenuated, but did not abolish, the antidiuretic action of angiotensin II. Significant decreases in urine formation by angiotensin II were observed, even in the presence of saralasin.These results suggest that nisoldipine, unlike saralasin, preferentially interferes with the stimulatory effect of angiotensin II, as related to the renal tubular reabsorption of sodium and water.

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“…There are a number of reports which show that the calcium entry blocking drugs have an action on the kidney to increase the excretion of sodium and water in experimental animals (Bell & Lindner, 1984;Dietz et al, 1983;Johns, 1985) and man (Zanchetti & Leonetti, 1985). The exact way in which these compounds alter the reabsorption of sodium and water is not known, but it could result from their action on renal haemodynamics, to increase renal blood flow, or 'Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

Johns

Manitius

1986

British J Pharmacology

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1In pentobarbitone-anaesthetized rats, intravenous administration of diltiazem at 5 g kg-' min -' did not change blood pressure or renal blood flow but increased glomerular filtration rate by approximately 16%, urine flow by 85%, calcium excretion by 151% and absolute and fractional sodium excretions by 100% and 69%, respectively. A similar pattern of responses was obtained in renally denervated animals, except that calcium excretion did not change statistically. Diltiazem given at 20 pg kg'1 min-' into renally innervated and denervated groups of animals depressed blood pressure between 15-17 mmHg but had no effect on renal haemodynamic or tubular function. 2 Nitrendipine administered at 0.5 ig kg-' min-' to renally innervated and denervated animals significantly depressed blood pressure in intact animals by 6 mmHg and in both groups did not change renal haemodynamics but caused similar increases in urine flow ofbetween 79-98%, calcium excretion of between 87 and 125%, absolute sodium excretion of between 108 and 140% and fractional sodium excretion of between 83 and 170%. Infusion of nitrendipine at 1.0 jig kg-' min' into intact or renally denervated animals decreased blood pressure by 18-20 mmHg and increased urine flow by 84-111 %, calcium excretion by 85%, absolute sodium excretion by 81-137% and fractional sodium excretion by 52-102%. 3 Stimulation of the renal nerves at low frequencies (0.8 to 1.5 Hz) caused minimal changes in renal haemodynamics but decreased urine flow by 27%, calcium excretion by 35%, absolute and fractional sodium excretions 32% and 36%, respectively. In different groups of animals given either diltiazem at 20 pg kg-I min' or nitrendipine at 0.5 pg kg'-min' or 1.0 fg kg'-min' , a similar degree of renal nerve stimulation caused an identical pattern of excretory responses of similar magnitude to those obtained in the absence of drug. 4 The calciuretic, diuretic and natriuretic activities of diltiazem and nitrendipine were not dependent on renal nerves and probably represented a direct action on the tubular reabsorptive processes of these ions. The renal nerve-induced increases in tubular calcium and sodium reabsorption indicate that these a-adrenoceptor-mediated responses are not dependent on the inward movement of calcium

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Effects of Verapamil and Nifedipine on Renal Function and Hemodynamics in the Dog

Cited by 39 publications

References 26 publications

Multiple effects of calcium entry blockers on renal function in hypertension.

Multiple effects of calcium entry blockers on renal function in hypertension.

Inhibitory effects of nisoldipine and saralasin on angiotensin II-induced antidiuresis in anesthetized dogs.

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

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