Renal actions of calcium antagonists.

Calcium antagonists (CAs) interfere with the calcium entry of many cells and therefore affect various cells and properties of the kidney. At present, most information on the renal actions of CAs concerns their relaxing effects on vascular smooth muscle cells. Renal vasodilation and decreased renal vascular resistance are most prominent when CAs are used in hypertensive laboratory animals or patients. This results in an increase of renal blood flow and, at times, in an even greater rise of glomerular filtration rate (GFR). The augmenting effect on GFR is at present incompletely understood. It has been considered that it is due to the rise of the glomerular capillary pressure and/or due to increase of the glomerular capillary ultrafiltration coefficient. Unlike other vasodilators, CAs do not cause fluid retention, but rather induce diuresis and natriuresis. Initial studies on the renal effects of CAs in states of hypertension and/or impaired kidney function have demonstrated that CAs may play a role in maintaining GFR in otherwise progressive kidney disease. It remains to be seen whether these effects are related not only to the improvement of renal hemodynamics but also to protection against the action of inflammatory cells such as macrophages and platelets. While CAs have gained an established role in the treatment of hypertension showing beneficial short-term action on the kidneys, their long-term effects on renal structures and function require further elucidation.