Abstract :
Calcium antagonists have assumed a very important role as antihypertensive agents. In addition to efficacy, their metabolic neutrality (including the fact that they do not exacerbate dyslipidemia) comments their use. An increasing body of evidence is accruing to suggest that calcium antagonists may have renal protective effects, which is an additional factor favoring their use in treating hypertension. Despite their inability to lower glomerular capillary pressure directly, calcium antagonists lessen injury in many experimental models of renal disease, by retarding renal growth and countervailing or attenuating the mitogenic effects of diverse growth factors (Kidney Int 1992;41:S66-S72). Nevertheless, concerns have arisen recently regarding potential adverse effects of dihydropyridines. Thus, controversy exists about whether or not calcium antagonists exacerbate proteinuria, and secondly, whether some chemical subclasses are more apt to induce this. We have critically reviewed (Arch Int Med 1994;154:1185-1202) the available reports and noted that the results vary markedly, precluding rigorous inferences. A recent rigorous short-term study characterizing the effects of nifedipine on glomerular hemodynamics, sieving function, and protein excretion disclosed that nifedipine has no effect on albuminuria and glomerular barrier function but inhibits proximal tubular function. A wide experience indicates that calcium antagonists can be used safely in a broad range of patients, both blacks and whites, and with commonly encountered concomitant disorders including COPD, diabetes, peripheral vascular disease, and abnormal lipid profiles. At this juncture, with the current state of knowledge one may conclude that calcium antagonists are very important agents for first line monotherapy for hypertension.
