Effect of calcium channel blockers on intracellular calcium accumulation

Protection against acute renal failure by calcium channel blockers include radiocontrast agent, cyclosporin, aminoglycosides, amphotericin B, cisplatin nephrotoxicity, and ischaemia-induced toxicity. Calcium overload occurs in ischaemic cells. The type of calcium channel blocker influences the potential effect on protection against nephrotoxicity. A number of growth factors and hormones induce cellular activation by increasing calcium concentrations. Calcium channel blockers interfere with activation of different cell types, e.g. decrease platelet aggregation, macrophage activation, platelet-activating factor release and also proliferative response of vascular smooth muscle and mesangial cells. Uraemia is also a state of calcium accumulation. Increase of intracellular calcium [Ca2+]i in PMNLs is associated with deactivation. Treatment with calcium channel blockers normalizes elevated PMNL [Ca2+]i and improves functional parameters of PMNLs. Normalization of enhanced [Ca2+]i of PMNLs can also be achieved with effective 1,25(OH)2 vitamin D3 therapy by lowering PTH. Uraemia is also a state of insulin resistance. Elevated levels of [Ca2+]i in insulin target cells diminish sensitivity to insulin at the postbinding site. Therapeutic manoeuvres preventing the increase of cytosolic calcium may improve insulin resistance.