During the past decade, considerable attention has been focused on the effects of calcium antagonists on renal function. Direct in vivo and in vitro observations in diverse experimental models indicate that calcium antagonists antagonize preglomerular vasoconstriction. Furthermore, calcium antagonists are postulated to have additional properties that contribute to their ability to afford renal protection. These putative mechanisms include the ability to retard renal growth, and possibly to attenuate mesangial entrapment of macromolecules, and to attenuate the mitogenic effects of diverse growth factors. Although the clinical implications of the above-mentioned findings have not been fully delineated, the results of recent clinical trials indicate that calcium antagonists exert salutary effects on renal function in clinical settings characterized by impaired renal hemodynamics, including transplant-associated acute renal insufficiency and, possibly, cyclosporine nephrotoxicity. Evidence has accrued suggesting that calcium antagonists may also be protective against acute radiocontrast-induced nephrotoxicity. Finally, the renal hemodynamic and natriuretic effects of calcium antagonists commend their use as antihypertensive agents in the management of essential hypertension, renovascular hypertension, and transplant-associated hypertension.
Murray Epstein (1992) studied this question.