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This Article Full Text Full Text (PDF) All Versions of this Article: 289/3/H1277    most recent 01052.2004v1 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 (8) Citing Articles via Google Scholar Google Scholar Articles by Bratz, I. N. Articles by Kanagy, N. L. Search for Related Content PubMed PubMed Citation Articles by Bratz, I. N. Articles by Kanagy, N. L.

Reduced molecular expression of K⁺ channel proteins in vascular smooth muscle from rats made hypertensive with N-nitro-L-arginine

¹Department of Physiology, Louisiana State University Health Science Center, New Orleans, Louisiana; and ²Cell Biology and Physiology Department and ³Neurosciences Department, University of New Mexico School of Medicine, Albuquerque, New Mexico

Submitted 13 October 2004 ; accepted in final form 14 March 2005

Smooth muscle membrane potential (E_m) depends on K⁺ channels, and arteries from rats made hypertensive with N-nitro-L-arginine (LHR) are depolarized compared with control. We hypothesized that decreased K⁺ channel function, due to decreased K⁺ channel protein expression, underlies E_m depolarization. Furthermore, K⁺ channel blockers should move control E_m (–46 ± 1 mV) toward that in LHR (–37 ± 2 mV) and normalize contraction. The E_m vs. K⁺ relationship was less steep in LHR (23 ± 2 vs. 28 ± 1 mV/log K⁺ concentration), and contractile sensitivity to K⁺ was increased (EC₅₀ = 37 ± 1 vs. 23 ± 1 mM). Iberiotoxin (10 nM), an inhibitor of large-conductance Ca²⁺-activated K⁺ (BK_Ca) channels, depolarized control and LHR E_m to –35 ± 1 and –30 ± 2 mV, respectively; however, effects on K⁺ sensitivity were more profound in LHR (EC₅₀ = 25 ± 2 vs. 15 ± 3 mM). The voltage-dependent K⁺ (K_V) channel blocker 4-aminopyridine (3 mM) depolarized control E_m to the level of LHR (–28 ± 1 vs. –28 ± 1 mV); however, effects on K⁺ sensitivity were greater in LHR (EC₅₀ = 17 ± 4 vs. 4 ± 4 mM). Western blots revealed reduced BK_Ca and K_V1.5 channel expression in LHR arteries. The findings suggest that diminished expression of K⁺ channels contributes to depolarization and enhanced contractile sensitivity. These conclusions are supported by direct electrophysiological assessment of BK_Ca and K_V channel function in control and LHR smooth muscle cells [see companion paper (Bratz IN, Swafford AN Jr, Kanagy NL, and Dick GM. Am J Physiol Heart Circ Physiol 289: H1284–H1290, 2005)].

nitric oxide; membrane potential; iberiotoxin; 4-aminopyridine

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