Vasoconstriction triggered by hydrogen sulfide: Evidence for Na,K,2Clcotransport and L-type Ca channel-mediated pathway.

Objectives: This study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC).

Methods: Isometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na/K-pump and Na,K,2Clcotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the Rb influx, respectively.

[Ionic mechanisms of carbon monoxide action on the contractile properties of smooth muscles of the blood vessels].

Carbon monoxide (CO) is one of a family of gas transmitters. In this article we present the results of mechanographic investigations of the mechanisms of CO action on a rat thoracic aorta segments. We found that relaxing effect of CO donor CORM-2 on vascular smooth muscles is mediated mainly by opening of voltage-dependent potassium channels in smooth muscle cells: 4-aminopyridine, blocking these channels, almost completely eliminated the CO-induced vasorelaxation of the segments precontracted by depolarization of the smooth muscle cells membranes with high potassium (30 mM KCl) solution or by phenylephrine (10 microM).