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This Article Full Text Full Text (PDF) All Versions of this Article: 289/3/H1284    most recent 01053.2004v1 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 (9) Citing Articles via Google Scholar Google Scholar Articles by Bratz, I. N. Articles by Dick, G. M. Search for Related Content PubMed PubMed Citation Articles by Bratz, I. N. Articles by Dick, G. M.

Reduced functional expression of K⁺ channels in vascular smooth muscle cells from rats made hypertensive with N-nitro-L-arginine

¹Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana; and ²Cell Biology and Physiology Department, University of New Mexico School of Medicine, Albuquerque, New Mexico

Submitted 13 October 2004 ; accepted in final form 4 May 2005

Smooth muscle membrane potential is determined, in part, by K⁺ channels. In the companion paper to this article (Bratz IN, Dick GM, Partridge LD, and Kanagy NL. Am J Physiol Heart Circ Physiol 289: H1277–H1283, 2005), we demonstrated that superior mesenteric arteries from rats made hypertensive with N-nitro-L-arginine (L-NNA) are depolarized and express less K⁺ channel protein compared with those from normotensive rats. In the present study, we used patch-clamp techniques to test the hypothesis that L-NNA-induced hypertension reduces the functional expression of K⁺ channels in smooth muscle. In whole cell experiments using a Ca²⁺-free pipette solution, current at 0 mV, largely due to voltage-dependent K⁺ (K_V) channels, was reduced 60% by hypertension (2.7 ± 0.4 vs. 1.1 ± 0.2 pA/pF). Current at +100 mV with 300 nM free Ca²⁺, largely due to large-conductance Ca²⁺-activated K⁺ (BK_Ca) channels, was reduced 40% by hypertension (181 ± 24 vs. 101 ± 28 pA/pF). Current blocked by 3 mM 4-aminopyridine, an inhibitor of many K_V channel types, was reduced 50% by hypertension (1.0 ± 0.4 vs. 0.5 ± 0.2 pA/pF). Current blocked by 1 mM tetraethylammonium, an inhibitor of BK_Ca channels, was reduced 40% by hypertension (86 ± 14 vs. 53 ± 19 pA/pF). Differences in BK_Ca current magnitude are not attributable to changes in single-channel conductance or Ca²⁺/voltage sensitivity. The data support the hypothesis that L-NNA-induced hypertension reduces K⁺ current in vascular smooth muscle. Reduced molecular and functional expression of K⁺ channels may partly explain the depolarization and augmented contractile sensitivity of smooth muscle from L-NNA-treated rats.

nitric oxide; membrane potential; Ca²⁺-activated K⁺ channel; delayed rectifier K⁺ channel; hypertension

This article has been cited by other articles:

				H. Xu, W. F. Jackson, G. D. Fink, and J. J. Galligan Activation of Potassium Channels by Tempol in Arterial Smooth Muscle Cells From Normotensive and Deoxycorticosterone Acetate-Salt Hypertensive Rats Hypertension, December 1, 2006; 48(6): 1080 - 1087. [Abstract] [Full Text] [PDF]

				I. N. Bratz, G. M. Dick, L. D. Partridge, and N. L. Kanagy Reduced molecular expression of K+ channel proteins in vascular smooth muscle from rats made hypertensive with N{omega}-nitro-L-arginine Am J Physiol Heart Circ Physiol, September 1, 2005; 289(3): H1277 - H1283. [Abstract] [Full Text] [PDF]