The current study investigates the mechanism by which the concentration of activator Ca2+ is decreased during potassium induced relaxation of vascular smooth muscle. Helically cut strips of rat tail artery were mounted between a fixed base and force transducers; isometric contractions were recorded. The arterial strips relaxed in response to potassium after contraction induced by norepinephrine in potassium-free solution. The efflux of 45Ca2+ from the strips was stimulated by norepinephrine during the potassium-free cycle. This increase in efflux was prevented during potassium induced relaxation. D-600, an inhibitor of transmembrane Ca2+ flux, reduced the magnitude of potassium induced relaxation by 35%. These observations suggest that relaxation in response to potassium is the result of a decrease in membrane permeability to Ca2+ coupled with an increase in Ca2+ sequestration at intracellular sites.
|Original language||English (US)|
|Number of pages||5|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - Jul 1980|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)