Renal effects of calcium antagonists with special reference to manidipine hydrochloride

The aim of this study was to review the effect of the calcium antagonists in general and manidipine hydrochloride in particular on the different renal haemodynamic parameters in experimental animals and human beings.

The paper includes data from experimental and human studies performed between 1978 and 1995.

As far as renal blood flow and glomerular filtration rate are concerned in experimental animals and in men, manidipine, a long-lasting dihydropyridine calcium antagonist, demonstrated its action not only on the afferent arteriole, as other dihydropyridines, but also on the efferent one. This action, which avoids producing any increase in intra-glomerular pressure and renal damage, would be similar to that of angiotensin converting enzyme inhibitors. The direct natriuretic effect of manidipine, observed also with other dihydropyridines, has been demonstrated by two studies performed in both spontaneously hypertensive and normotensive rats, indicating a direct renal tubular effect. In 5/6 nephrectomized rats treated with manidipine, blood pressure, proteinuria, serum creatinine and glomerular lesions, observed after histological examination, were significantly reduced with respect to control untreated 5/6 nephrectomized rats. Calcium antagonists have demonstrated a clear beneficial effect on renal vasoconstriction induced by cyclosporine therapy in renal transplant patients and in the prevention of acute renal failure secondary to the administration of radiocontrast agents, amphotoricin B, cisplatin and aminoglycosides.

Calcium antagonists are effective drugs for controlling blood pressure and for inducing renal vasodilatation. Manidipine hydrochloride increases renal blood flow and glomerular filtration rate with vasodilation of afferent as well as efferent arterioles, reducing intraglomerular pressure. According to experimental and human studies on renal haemodynamics, manidipine could be used in diabetic nephropathy, glomerular lesions, microalbuminuria and proteinuria.