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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on February 20, 2004; DOI: 10.1124/jpet.103.062810

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Received for publication November 18, 2003.
Revised February 12, 2004.
Accepted for publication February 19, 2004.

Ca2+-activated K+ channels underlying the impaired acetylcholine-induced vasodilation in 2K-1C Hypertensive rats

Glaucia E Callera 1*, Alvaro Yogi 1, Rita C Tostes 1, Luciana V Rossoni 1, Lusiane M Bendhack 1

1 University of Sao Paulo

* Address correspondence to: E-mail: elena-glaucia.callera{at}ircm.qc.ca

Abstract

We tested the hypothesis that an abnormal function of K+ channels in vascular smooth muscle cells plays a key role in the impaired acetylcholine (Ach) vasodilation in aortas from two kidney-one clip (2K-1C) hypertensive rats and further investigated the K+ channel subtype involved in this altered response. Ach-induced endothelium-dependent relaxation was assessed in aortic rings from 2K-1C and normotensive two kidney (2K) rats. Glibenclamide, an ATP-sensitive K+ channel blocker, did not inhibit Ach-induced relaxation in aortic rings from 2K or 2K-1C rats. The voltage-dependent K+ channels (KV) inhibitor 4-aminopyridine attenuated Ach-induced relaxation in both groups with a greater inhibitory effect in aortic rings from 2K-1C rats. Charybdotoxin and iberiotoxin, blockers of Ca2+-sensitive (KCa) and large-conductance KCa (BKCa) channels, respectively, reduced Ach-induced relaxation in aortic rings from 2K rats without affecting this response in those from 2K-1C rats, abolishing the differences between groups. Ach-induced relaxation in vessels from both 2K and 2K-1C rats was unaffected by apamin, a small-conductance KCa blocker. NS1619, an activator of KCa, induced a smaller vasodilation in endothelium-denuded aortic rings from 2K-1C rats compared with those from 2R rats. Iberiotoxin reduced sodium nitroprusside-induced relaxation in endothelium-denuded aortic rings from 2K without affecting this response in those from 2K-1C rats. The inhibition of Na+,K+-ATPase with ouabain had no effects on Ach-induced relaxation in aortic rings from 2K-1C or 2K rats. These data indicate that a deficient functional activity of BKCa channels plays a key role in the impaired Ach vasodilation in aortas from 2K-1C rats.


Key words: 2K-1C hypertension, Na+K+-ATPase, acetylcholine, potassium channels, vascular smooth muscle, vasodilation


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