Role of T-type Ca〔2+〕 Channels in Renal Microcirculation

DOI Web Site PubMed 被引用文献10件 参考文献66件
  • Hayashi Koichi
    Department of Internal Medicine, School of Medicine, Keio University
  • Wakino Shu
    Department of Internal Medicine, School of Medicine, Keio University
  • Homma Koichiro
    Department of Internal Medicine, School of Medicine, Keio University
  • Sugano Naoki
    Department of Internal Medicine, School of Medicine, Keio University
  • Saruta Takao
    Department of Internal Medicine, School of Medicine, Keio University

書誌事項

タイトル別名
  • Pathophysiological Significance of T-type Ca2+ Channels: Role of T-type Ca2+ Channels in Renal Microcirculation
  • Role of T type Ca 2 Channels in Renal Microcirculation

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Since conventional Ca2+ antagonists, with predominant blockade of L-type voltage-dependent Ca2+ channels, elicit preferential dilation of afferent arterioles, they might ostensibly aggravate glomerular hypertension. Recently, novel Ca2+ antagonists, with inhibitory action on L-/T-type Ca2+ channels, have been reported to dilate both afferent and efferent arterioles. The present review attempted to characterize the renal action of these Ca2+ antagonists and evaluated the consequences following the treatment with these agents. In contrast to conventional Ca2+ 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 Ca2+ 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, Ca2+ antagonists with T-type Ca2+ 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 Ca2+ 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.<br>

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