Intracellular smooth muscle [Ca2+] in acetylcholine and nitric oxide-mediated relaxation of human small arteries

European Journal of Pharmacology
Niels H BuusMichael J Mulvany

Abstract

In human resistance arteries the role of intracellular calcium during receptor agonist and nitric oxide (NO)-mediated vasorelaxation is almost unknown. We examined changes in smooth muscle calcium concentration ([Ca2+]i) caused by acetylcholine and the NO donor S-nitroso-N-acetylpenicillamine (SNAP) in isolated human subcutaneous small arteries. In arteries constricted with 50 mM KCl, acetylcholine and SNAP induced relaxation without any change in [Ca2+]i, whereas in noradrenaline constricted vessels, both acetylcholine and to a lesser degree also SNAP-mediated relaxation were associated with a decrease in [Ca2+]i. Furthermore incubation with SNAP (1 microM) induced a rightward shift in the [Ca2+]i-force relationship. These results suggest that relaxation mediated by endothelium derived hyperpolarizing factors (EDHF) is associated with reduction in [Ca2+]i, whereas NO-mediated relaxation can take place without changes in [Ca2+]i. This finding seems to be, at least partly, due to NO-mediated desensitization of the contractile apparatus to calcium.

References

Apr 1, 1992·Pflügers Archiv : European journal of physiology·P E JensenC Aalkjaer
Dec 1, 1995·Circulation·R A Cohen, P M Vanhoutte
Aug 31, 1999·Journal of Hypertension·P M Vanhoutte
Apr 7, 2004·British Journal of Pharmacology·Wendy W BatenburgA H Jan Danser

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Citations

Feb 2, 2008·Methods in Enzymology·Ian R Davies, Xueji Zhang

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