Effects of calcium antagonists on renal hemodynamics.
The renal hemodynamic effects of Ca2+ antagonists are considered in the context of their actions on Ca2+ movements during activation of vascular smooth muscle. Observations in intact animals reveal that the renal hemodynamic response to Ca2+ antagonists is highly variable, depending on the neural and hormonal determinants of renal vascular tone. Studies in the isolated perfused kidney and in isolated renal vessels indicate that diverse agonists use different activating mechanisms with differing sensitivities to Ca2+ antagonists. In comparison with other direct-acting vasodilators, Ca2+ antagonists are unique in their ability to maintain or increase glomerular filtration rate. This effect is due, in part, to their selective reduction of afferent arteriolar resistance. This implies that activating mechanisms of the afferent and efferent arterioles differ. The ability of Ca2+ antagonists to augment glomerular filtration rate by concomitant actions on nonvascular sites remains to be elucidated.
D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D005919:Glomerular Filtration Rate; D006439:Hemodynamics / Q000187:drug effects; D006706:Homeostasis; D006801:Humans; D066298:In Vitro Techniques; D007684:Kidney Tubules / Q000187:drug effects; D009129:Muscle Tonus / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D011189:Potassium Chloride; D012079:Renal Circulation / Q000187:drug effects*; D014661:Vasoconstriction
D002121:Calcium Channel Blockers; D011189:Potassium Chloride; D002118:Calcium