Verapamil Effect on Renal Function of Normotensive and Hypertensive Rats

MacLaughlin, M; Aires, Margarida de Mello; Malnic, Gerhard

doi:10.1159/000173042

Cited by 15 publications

(7 citation statements)

References 24 publications

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“…Nevertheless, in a micropuncture experiment, MacLaughlin et al 39 observed that 10" 5 M verapamil added to the luminalfluid perfusate of normal Wistar rats produced a 36% decrease of sodium reabsorption and that a greater reduction (61%) of sodium reabsorption occurred when verapamil was infused into peritubular capillaries. Similarly, Figueiredo et al 40 found a significant decrease of sodium reabsorption in isolated perfused proximal tubules of rabbits when verapamil was added to the bathing solution in a concentration of 5 /nmol/dl.…”

mentioning

confidence: 99%

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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mentioning

confidence: 99%

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

Romero

Raij²,

Granger

et al. 1987

Hypertension

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“…Consis tent with these findings, a previous in vivo micropuncture study in the rat demonstrated that the renal interstitial in fusion of 10 5 M PGE2 significantly stimulated proximal so dium reabsorption [6]. Additionally, a previous in vivo mi croperfusion study showed that 10 ' M verapamil added to the luminal fluid perfusate markedly decreased proximal sodium reabsorption [9], Therefore, the renal interstitial in fusions of verapamil and PGE: have opposing effects on so dium reabsorption by the proximal tubule of the rat.…”

Section: Discussionmentioning

confidence: 56%

Reversal of the Antinatriuretic Effect of Prostaglandin E<sub>2</sub> by Verapamil in the Rat

Peng¹,

Ramsey²,

Knox³

1996

Kidney Blood Press Res

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Previous studies have demonstrated that prostaglandin E₂ (PGE₂) infusion increases intrarenal angiotensin-II (ANG-II) formation and decreases sodium excretion in the rat. PGE₂ infusion may have direct tubular effects or indirect effects through increased intrarenal ANG-II. In the present study, the calcium channel blocker verapamil was used to determine whether it would reverse the PGE₂-induced decrease in sodium excretion. To minimize any systemic and hemodynamic influences, verapamil and PGE₂ were infused directly into the renal interstitium via a chronically implanted matrix. Fractional sodium excretion (FE_Na), glomerular filtration rate (GFR), mean arterial pressure (MAP), and plasma renin activity (PRA) were measured before and during renal interstitial infusion of PGE₂ (10^-5M) and/or verapamil (10^-3M) in rats pretreated with indomethacin. The renal interstitial infusion of PGE₂ alone significantly decreased FE_Na (Δ-1.0 ± 0.2%), whereas the addition of verapamil reversed the effect of PGE₂ and significantly increased FE_Na (Δ2.6 ± 0.3%, n = 9). The renal interstitial infusion of verapamil alone markedly increased FE_Na (△1.7 ± 0.3%, n = 7), and this natriuresis was accompanied by a significant decrease in PRA (Δ-0.6 ± 0.1 ng/ml/h, p < 0.05). The addition of PGE₂ to the interstitial infusion did not further affect FE_Na or PRA. There was a significant difference between the effect of interstitial PGE₂ infusion and interstitial verapamil infusion on PRA (Δ1.9 ± 0.8 vs. Δ-0.6 ± 0.1 ng/ml/h, p < 0.05). GFR and MAP remained unchanged in response to the renal interstitial infusion of PGE₂ and/or verapamil. In conclusion, verapamil reversed the PGE₂-induced antinatriuresis in the rat.

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“…18 observed that 5-10 mol verapamil added to the luminal perfusate of normal Wistar rats caused a 36% decrease of Na reabsorption. When verapamil was infused into the peritubular capillaries a greater reduction of 61% of Na reabsorption occurred.…”

Section: Discussionmentioning

confidence: 96%

Calcium entry blocker nicardipine inhibits sodium and inorganic phosphate reabsorption independent of renal circulation in dogs

Goto

Watanabe

1992

J Anesth

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The effects of nicardipine on renal function were studied in anesthetized dogs. The changes in the tubular sodium (Na) and inorganic phosphate (PO(4)) reabsorption caused by the drug infusion into the renal artery without altered systemic and real circulation were especially evaluated. In dogs receiving a smaller dose of nicardipine (5 ng.kg(-1).min(-1)) into the left renal artery the blood pressure and renal circulation did not change, but urine volume and urinary Na and PO(4) excretion increased significantly. In dogs receiving a larger dose of nicardipine (50 ng.kg(-1).min(-1)) into the renal artery, renal plasma flow, urine volume and urinary Na and PO(4) excretion increased significantly, but creatinine clearance did not. The fractional distal Na reabsorption did not change with nicardipine infusion in either group. PO(4) reabsorption is considered to occur mainly in the proximal renal tubule, so its appearance in urine in increased quantities without the changes of systemic and renal circulation suggests proximal activity of the drug.

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Verapamil Effect on Renal Function of Normotensive and Hypertensive Rats

Cited by 15 publications

References 24 publications

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

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

Reversal of the Antinatriuretic Effect of Prostaglandin E<sub>2</sub> by Verapamil in the Rat

Calcium entry blocker nicardipine inhibits sodium and inorganic phosphate reabsorption independent of renal circulation in dogs

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