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Am J Physiol Renal Physiol (February 15, 2005). doi:10.1152/ajprenal.00353.2004
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Submitted on September 20, 2004
Accepted on January 27, 2005

Raloxifene relaxes rat intrarenal arteries by inhibiting Ca2+ influx

Fung Ping Leung1, Xiaoqiang Yao1, Chi-Wai Lau1, Wing-Hung Ko1, Limin Lu2, and Yu Huang1*

1 Department of Physiology, Chinese University of Hong Kong, Hong Kong, Hong Kong
2 Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai, China

* To whom correspondence should be addressed. E-mail: yu-huang{at}cuhk.edu.hk.

Raloxifene may confer vascular benefits without causing estrogen-related side effects. However, its action on renal vascular circulation is unknown. This study aimed to examine the sex difference and roles of endothelium and Ca2+ channels in the rat renovascular relaxation to raloxifene. On isolated intralobar renal artery rings mounted in a myograph and contracted by U46619, concentration-relaxation curves were constructed for raloxifene and contractions to CaCl2 were studied. Changes in intracellular Ca2+ levels ([Ca2+]i) of vascular smooth muscle (VSM) were measured by Fura-2 fluorescence. Raloxifene or 17{beta}-estradiol was equally effective in relaxing renal artery from both sexes with raloxifene being more potent than 17{beta}-estradiol. Endothelial denudation did not affect raloxifene-or 17{beta}-estradiol-induced relaxation. NG-nitro-L-arginine methyl ester, charybdotoxin plus apamin, indomethacin, or ICI 182,780 did not modify the effect of raloxifene. Raloxifene caused similar relaxations in rings contracted by U46619 and high K+. Nifedipine attenuated the potency of raloxifene. Raloxifene reduced CaCl2-induced contractions. 80 mM K+ stimulated an increase in VSM [Ca2+]i and raloxifene attenuated this effect. Raloxifene-induced reduction in contraction and increase in VSM [Ca2+]i was insensitive to ICI 182,780. In summary, raloxifene causes relaxation in rat renal arteries; this effect is independent of a functional endothelium and is not mediated by ICI 182,780-sensitive estrogen receptors. Raloxifene inhibited both contractions and VSM [Ca2+]i in response to CaCl2, indicating that raloxifene relaxes rat renal arteries primarily through inhibiting Ca2+ influx via Ca2+ channels. There is little sex difference in raloxifene-induced relaxation.




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