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Pharmacology of ATP-sensitive K+ currents in smooth muscle cells from rabbit mesenteric artery.

Quayle J, Bonev A, Brayden J, Nelson MT

American Journal of Physiology-Cell Physiology. 1995;269( 5 Pt 1):C1112-8.

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Abstract

The inference that ATP-sensitive K+ (KATP) channels are involved in arterial responses to the synthetic K+ channel openers, hypoxia, adenosine, and calcitonin gene-related peptide, has relied on the sensitivity of these responses to the sulfonylureas glibenclamide and tolbutamide and to tetraethylammonium (TEA+). The inhibition of KATP currents by glibenclamide, tolbutamide, and TEA+ was investigated in single smooth muscle cells from rabbit mesenteric artery by use of the whole cell patch-clamp technique. The synthetic K+ channel openers pinacidil (half-activation 0.6 microM), cromakalim (half-activation 1.9 microM), and diazoxide (half-activation 37.1 microM) activated K(+)-selective currents that were blocked by glibenclamide. Elevation of pipette (intracellular) ATP concentration decreased K+ currents induced by pinacidil. Half-inhibition of KATP currents by glibenclamide and tolbutamide occurred at 101 nM and 351 microM, respectively. KATP currents were also inhibited by external TEA+, with half-inhibition at 6.2 mM. The results indicate that glibenclamide is an effective inhibitor of KATP channels in arterial smooth muscle and that tolbutamide and TEA+ are much less effective. Furthermore, these results support numerous functional studies that have demonstrated that the vasorelaxations to K+ channel openers are inhibited by < 10 microM glibenclamide but not by < 1 mM TEA+.

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UNITED STATES
Volume:
269( 5 Pt 1)
Start page:
C1112
End page:
8
Pagination:
C1112-8
Access state:
Active

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Manchester eScholar ID:
uk-ac-man-scw:1d16434
Created:
30th August, 2009, 13:57:27
Last modified:
3rd March, 2010, 17:09:02

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