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lüll Pathophysiological significance of T-type Ca2+ channels: role of T-type Ca2+ channels in renal microcirculation Hayashi K; Wakino S; Homma K; Sugano N; Saruta TJ Pharmacol Sci 2005[Nov]; 99 (3): 221-7Since conventional Ca(2+) antagonists, with predominant blockade of L-type voltage-dependent Ca(2+) channels, elicit preferential dilation of afferent arterioles, they might ostensibly aggravate glomerular hypertension. Recently, novel Ca(2+) antagonists, with inhibitory action on L-/T-type Ca(2+) channels, have been reported to dilate both afferent and efferent arterioles. The present review attempted to characterize the renal action of these Ca(2+) antagonists and evaluated the consequences following the treatment with these agents. In contrast to conventional Ca(2+) antagonists (e.g., nifedipine), novel antagonists (e.g., benidipine, efonidipine) potently dilated afferent and efferent arterioles; their action on efferent arterioles appeared to be mediated by the T-type Ca(2+) channel blockade, probably through the inhibition of the intracellular Ca(2+) release. The comparison of the anti-proteinuric action in subtotally nephrectomized rats showed that efonidipine exerted more prominent action than nifedipine. Furthermore, Ca(2+) antagonists with T-type Ca(2+) inhibitory action inhibited renin/aldosterone release and proinflammatory process. Finally, patients with chronic renal disease given a 48-week efonidipine treatment showed reduced proteinuria, and this effect was seen even when mean arterial blood pressure failed to become less than 100 mmHg. Collectively, T-type Ca(2+) channel blockade provides beneficial action in renal injury. Various mechanisms serve to protect against renal injury, including systemic/glomerular hemodynamic action and non-hemodynamic mechanisms.|Animals[MESH]|Calcium Channel Blockers/pharmacology[MESH]|Calcium Channels, T-Type/*physiology[MESH]|Calcium/antagonists & inhibitors[MESH]|Dihydropyridines/therapeutic use[MESH]|Humans[MESH]|Kidney Diseases/drug therapy[MESH]|Kidney/*blood supply[MESH]|Microcirculation[MESH]|Nitrophenols/therapeutic use[MESH]|Organophosphorus Compounds/therapeutic use[MESH]|Renal Circulation/*physiology[MESH]|Signal Transduction[MESH] |