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Renal Microcirculation and Calcium Channel Subtypes

It has recently been reported that voltage-dependent Ca channel subtypes, e.g., L-, T-, N-, and P/Q-type, are expressed in renal arterioles and renal tubules, and the inhibition of these channels exerts various effects on renal microcirculation. For example, selective blockade of L-type Ca channels...

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Autores principales: Homma, Koichiro, Hayashi, Koichi, Yamaguchi, Shintaro, Fujishima, Seitaro, Hori, Shingo, Itoh, Hiroshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033552/
https://www.ncbi.nlm.nih.gov/pubmed/24479750
http://dx.doi.org/10.2174/1573402110666140131160617
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author Homma, Koichiro
Hayashi, Koichi
Yamaguchi, Shintaro
Fujishima, Seitaro
Hori, Shingo
Itoh, Hiroshi
author_facet Homma, Koichiro
Hayashi, Koichi
Yamaguchi, Shintaro
Fujishima, Seitaro
Hori, Shingo
Itoh, Hiroshi
author_sort Homma, Koichiro
collection PubMed
description It has recently been reported that voltage-dependent Ca channel subtypes, e.g., L-, T-, N-, and P/Q-type, are expressed in renal arterioles and renal tubules, and the inhibition of these channels exerts various effects on renal microcirculation. For example, selective blockade of L-type Ca channels with nifedipine preferentially dilates the afferent arteriole and potentially induces glomerular hypertension. On the other hand, recently developed Ca channel blockers (CCBs) such as mibefradil and efonidipine block both T-type and L-type Ca channels and consequently dilate both afferent and efferent arterioles, leading to lowering of intraglomerular pressure. Interestingly, aldosterone has recently been recognized as a factor exacerbating renal diseases, and its secretion from adrenal gland is mediated by T-type Ca channels. Furthermore, T-type CCBs were shown to ameliorate renal dysfunction by suppressing inflammatory processes and renin secretion. On the basis of histological evaluations, N-type Ca channels are present in peripheral nerve terminals innervating both afferent and efferent arterioles. Further, it was suggested that N-type CCBs such as cilnidipine suppress renal arteriolar constriction induced by enhanced sympathetic nerve activity, thereby lowering intraglomerular pressure. Taken together, various Ca channel subtypes are present in the kidney and blockade of selective channels with distinct CCBs exerts diverse effects on renal microcirculation. Inhibition of T-type and N-type Ca channels with CCBs is anticipated to exert pleiotropic effects that would retard the progression of chronic kidney disease through modulation of renal hemodynamic and non-hemodynamic processes.
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spelling pubmed-40335522014-05-27 Renal Microcirculation and Calcium Channel Subtypes Homma, Koichiro Hayashi, Koichi Yamaguchi, Shintaro Fujishima, Seitaro Hori, Shingo Itoh, Hiroshi Curr Hypertens Rev Article It has recently been reported that voltage-dependent Ca channel subtypes, e.g., L-, T-, N-, and P/Q-type, are expressed in renal arterioles and renal tubules, and the inhibition of these channels exerts various effects on renal microcirculation. For example, selective blockade of L-type Ca channels with nifedipine preferentially dilates the afferent arteriole and potentially induces glomerular hypertension. On the other hand, recently developed Ca channel blockers (CCBs) such as mibefradil and efonidipine block both T-type and L-type Ca channels and consequently dilate both afferent and efferent arterioles, leading to lowering of intraglomerular pressure. Interestingly, aldosterone has recently been recognized as a factor exacerbating renal diseases, and its secretion from adrenal gland is mediated by T-type Ca channels. Furthermore, T-type CCBs were shown to ameliorate renal dysfunction by suppressing inflammatory processes and renin secretion. On the basis of histological evaluations, N-type Ca channels are present in peripheral nerve terminals innervating both afferent and efferent arterioles. Further, it was suggested that N-type CCBs such as cilnidipine suppress renal arteriolar constriction induced by enhanced sympathetic nerve activity, thereby lowering intraglomerular pressure. Taken together, various Ca channel subtypes are present in the kidney and blockade of selective channels with distinct CCBs exerts diverse effects on renal microcirculation. Inhibition of T-type and N-type Ca channels with CCBs is anticipated to exert pleiotropic effects that would retard the progression of chronic kidney disease through modulation of renal hemodynamic and non-hemodynamic processes. Bentham Science Publishers 2013-08 2013-08 /pmc/articles/PMC4033552/ /pubmed/24479750 http://dx.doi.org/10.2174/1573402110666140131160617 Text en © 2012 Bentham Science Publishers http://creativecommons.org/licenses/by/2.5/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Article
Homma, Koichiro
Hayashi, Koichi
Yamaguchi, Shintaro
Fujishima, Seitaro
Hori, Shingo
Itoh, Hiroshi
Renal Microcirculation and Calcium Channel Subtypes
title Renal Microcirculation and Calcium Channel Subtypes
title_full Renal Microcirculation and Calcium Channel Subtypes
title_fullStr Renal Microcirculation and Calcium Channel Subtypes
title_full_unstemmed Renal Microcirculation and Calcium Channel Subtypes
title_short Renal Microcirculation and Calcium Channel Subtypes
title_sort renal microcirculation and calcium channel subtypes
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033552/
https://www.ncbi.nlm.nih.gov/pubmed/24479750
http://dx.doi.org/10.2174/1573402110666140131160617
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