Why the study?
Does benidipine affect urine volume, electrolyte excretion, and renal hemodynamics in spontaneously hypertensive rats?
Does benidipine affect urine volume, electrolyte excretion, and renal hemodynamics in spontaneously hypertensive rats?
Benidipine induces diuresis and natriuresis and dilates both afferent and efferent glomerular arterioles in hypertensive rats, suggesting a renoprotective profile.
Hypothesis-generating for renoprotective effects in hypertension; leaves open clinical translation pending human data.
Effects of benidipine on urine volume, excretion of electrolytes and renal hemodynamics were investigated in anesthetized spontaneously hypertensive rats (SHR). Benidipine at 3 and 10 micrograms/kg (i.v.) significantly increased urine volume, sodium (Na) and potassium (K) excretion with no change of creatinine clearance (CCRE). The increase in K excretion was relatively slight when compared with that in Na excretion. In another series of experiments, the tubular sites of action of benidipine were determined by the lithium clearance (CLi) technique and the stop-flow method. Benidipine at 3 micrograms/kg (i.v.) increased CLi, decreased creatinine concentration and increased Na concentration in the stop-flow urine from the distal nephron. These results suggest that benidipine produces diuresis and natriuresis by the inhibition of water and Na reabsorption at both the proximal tubule and the distal nephron. Benidipine increased p-aminohippuric acid clearance, but not CCRE, at doses of 3 and 10 micrograms/kg (i.v.), suggesting that benidipine dilates the glomerular efferent arteriole as well as the afferent arteriole. It is, therefore, expected that benidipine does not cause intraglomerular hypertension and has a beneficial effect in progressive renal disease.
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Kusaka et al. (1994) studied this question.
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