Ca<sup>2+</sup>Channel Subtypes and Pharmacology in the Kidney

DOI Web Site PubMed 被引用文献16件 オープンアクセス
  • Koichi Hayashi
    From the Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
  • Shu Wakino
    From the Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
  • Naoki Sugano
    From the Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
  • Yuri Ozawa
    From the Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
  • Koichiro Homma
    From the Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
  • Takao Saruta
    From the Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan

書誌事項

公開日
2007-02-16
DOI
  • 10.1161/01.res.0000256155.31133.49
公開者
Ovid Technologies (Wolters Kluwer Health)

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説明

<jats:p>A large body of evidence has accrued indicating that voltage-gated Ca<jats:sup>2+</jats:sup>channel subtypes, including L-, T-, N-, and P/Q-type, are present within renal vascular and tubular tissues, and the blockade of these Ca<jats:sup>2+</jats:sup>channels produces diverse actions on renal microcirculation. Because nifedipine acts exclusively on L-type Ca<jats:sup>2+</jats:sup>channels, the observation that nifedipine predominantly dilates afferent arterioles implicates intrarenal heterogeneity in the distribution of L-type Ca<jats:sup>2+</jats:sup>channels and suggests that it potentially causes glomerular hypertension. In contrast, recently developed Ca<jats:sup>2+</jats:sup>channel blockers (CCBs), including mibefradil and efonidipine, exert blocking action on L-type and T-type Ca<jats:sup>2+</jats:sup>channels and elicit vasodilation of afferent and efferent arterioles, which suggests the presence of T-type Ca<jats:sup>2+</jats:sup>channels in both arterioles and the distinct impact on intraglomerular pressure. Recently, aldosterone has been established as an aggravating factor in kidney disease, and T-type Ca<jats:sup>2+</jats:sup>channels mediate aldosterone release as well as its effect on renal efferent arteriolar tone. Furthermore, T-type CCBs are reported to exert inhibitory action on inflammatory process and renin secretion. Similarly, N-type Ca<jats:sup>2+</jats:sup>channels are present in nerve terminals, and the inhibition of neurotransmitter release by N-type CCBs (eg, cilnidipine) elicits dilation of afferent and efferent arterioles and reduces glomerular pressure. Collectively, the kidney is endowed with a variety of Ca<jats:sup>2+</jats:sup>channel subtypes, and the inhibition of these channels by their specific CCBs leads to variable impact on renal microcirculation. Furthermore, multifaceted activity of CCBs on T- and N-type Ca<jats:sup>2+</jats:sup>channels may offer additive benefits through nonhemodynamic mechanisms in the progression of chronic kidney disease.</jats:p>

収録刊行物

  • Circulation Research

    Circulation Research 100 (3), 342-353, 2007-02-16

    Ovid Technologies (Wolters Kluwer Health)

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