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This Article Full Text Full Text (PDF) All Versions of this Article: 291/1/H216    most recent 01383.2005v2 01383.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Hilgers, R. H. P. Articles by Webb, R. C. Search for Related Content PubMed PubMed Citation Articles by Hilgers, R. H. P. Articles by Webb, R. C.

Regional heterogeneity in acetylcholine-induced relaxation in rat vascular bed: role of calcium-activated K⁺ channels

Department of Physiology, Medical College of Georgia, Augusta, Georgia

Submitted 30 December 2005 ; accepted in final form 8 February 2006

Ca⁺-activated K⁺-channels (K_Ca) regulate vasomotor tone via smooth muscle hyperpolarization and relaxation. The relative contribution of the endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation differs depending on vessel type and size. It is unknown whether these K_Ca channels are differentially distributed along the same vascular bed and hence have different roles in mediating the EDHF response. We therefore assessed the role of small- (SK_Ca), intermediate- (IK_Ca), and large-conductance (BK_Ca) channels in mediating acetylcholine-induced relaxations in both first- and fourth-order side branches of the rat superior mesenteric artery (MA1 and MA4, respectively). Two-millimeter segments of each MA were mounted in the wire myograph, incubated with N-nitro-L-arginine methyl ester (L-NAME, 100 µmol/l) and indomethacin (10 µmol/l), and precontracted with phenylephrine (10 µmol/l). Cumulative concentration-response curves to ACh (0.001–10 µmol/l) were performed in the absence or presence of selective K_Ca channel antagonists. Apamin almost completely abolished these relaxations in MA4 but only partially blocked relaxations in MA1. The selective IK_Ca channel blocker 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34) caused a significantly greater inhibition of the ACh-induced relaxation in MA4 compared with MA1. Iberiotoxin had no inhibitory effect in MA4 but blunted relaxation in MA1. Relative mRNA expression levels of SK_Ca (rSK1, rSK3, and rSK4 = rIK1) were significantly higher in MA4 compared with MA1. BK_Ca (rBK₁ and rBK₁) genes were similar in both MA1 and MA4. Our data demonstrate regional heterogeneity in SK_Ca and IK_Ca function and gene expression and stress the importance of these channels in smaller resistance-sized arteries, where the role of EDHF is more pronounced.

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