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A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1254/jphs.fmj05002x6 http://scihub22266oqcxt.onion/10.1254/jphs.fmj05002x6 16293936!ä!16293936 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=16293936&cmd=llinks): Failed to open stream: HTTP request failed! 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Pathophysiological significance of T-type Ca2+ channels: role of T-type Ca2+ channels in renal microcirculation |pdf=|usr=}}{{16293936}} gab.com Text Pathophysiological significance of T-type Ca2+ channels: role of T-type Ca2+ channels in renal microcirculation JO: J Pharmacol Sci http://www.kidney.de/pget.php?&tw=1&pmid=16293936 #FOAvip Since 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. Twit Text FOAVip Pathophysiological significance of T-type Ca2+ channels: role of T-type Ca2+ channels in renal microcirculation ????J Pharmacol Sci http://www.kidney.de/pget.php?&tw=1&pmid=16293936 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=16293936 #FOAvip English Wikipedia <ref>{{Cite pmid|16293936}}</ref> Pathophysiological significance of T-type Ca2+ channels: role of T-type Ca2+ channels in renal microcirculation #MMPMID16293936 Hayashi K; Wakino S; Homma K; Sugano N; Saruta T J Pharmacol Sci 2005[Nov]; 99 (3): 221-7 PMID16293936show ga Since 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]Pathophysiological significance of T-type Ca2+ channels: role of T-typ(epmc).pdf DeepDyve Pubget Overpricing