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Vol. 285, Issue 1, 293-298, April 1998
Franz Volhard Clinic and the Max-Delbrück Center for
Molecular Medicine (R.B., M.G., T.S., C.R., F.C.L., H.H.),
Virchow
University Hospitals, I. Medical Clinic (R.B., T.S.), Charité
University Hospital, Humboldt University of Berlin, Berlin, Germany
In some but not all arterial beds, smooth muscle cell calcium-activated
K+ channels (KCa channels) play a central role
in the mediation of the vasodilator response to nitric oxide (NO) and
other nitrates. We investigated the effect of nitrates on
KCa channels in the relaxation of human coronary arteries
by means of isometric contraction experiments in arterial rings. We
also measured whole-cell currents in freshly isolated human coronary
artery vascular smooth muscle cells via the patch-clamp
technique. Sodium nitroprusside, diethylamine-nitric oxide complex
sodium salt and isosorbide mononitratre completely relaxed rings
preconstricted with 5 µM serotonin and produced dose-dependent
relaxations of 5 µM serotonin-preconstricted human rings. The
relaxations were inhibited by
2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-oxyl 3-oxide (10 µM), which neutralizes nitric oxide. The KCa channel blockers iberiotoxin (100 nM) and tetraethylammonium ions (1 mM) significantly inhibited SNP-induced relaxations of human coronary arteries. Moreover, in the patch-clamp experiments, SNP (1 µM) stimulated KCa currents and spontaneous transient outward
K+ currents carried by Ca spark activated KCa
channels. The SNP-induced (1 µM) KCa current was strongly
inhibited by iberiotoxin (100 nM). These data show that activation of
KCa channels in smooth muscle cells contributes to the
vasodilating actions of nitrates and nitric oxide in human coronary
arteries. This finding may have unique clinical significance for the
development of antianginal and antihypertensive drugs that selectively
target K+ channels and Ca sparks..
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