Original Article

Effects of hydrochlorothiazide on contraction and 86Rb efflux in rat aorta

Gui-Song Wang, Yun-Shan Li, Shao-Xuan Fu


Hydrochlorothiazide (HCT) (0.1, 0.3 mmol.L-1) inhibited the contraction of rat aortic strips induced by low (< 40 mmol.L-1), not higher concentrations of KCl. HCT (0.3 mmol.L-1) did not inhibit the CaCl2-induced contraction of the aortic strips depolarized with high K+ (KCl 80 mmol.L-1). The inhibitory effect of HCT (0.1 mmol.L-1) on KCl (20 mmol.L-1)-induced contraction was markedly antagonized by BaCl2 (0.1 mmol.L-1) and tetraethylammonium (TEA) (0.3 mmol.L-1), but not by glibenclamide (Gli, 0.01 mmol.L-1). With norepinephrine (NE) or 5-HT as agonists, HCT (0.3 mmol.L-1) also inhibited the contractions of rat aortic strips. In the 2 components of NE-induced contraction, HCT inhibited only the tonic component depending on Ca2+ influx, but not the phasic component elicited by the release of intracellular Ca2+. The inhibitory action of HCT was endothelium-independent. That the HCT (3 mmol.L-1) increased the 86Rb efflux rate coefficient was antagonized by BaCl2 (0.1 mmol.L-1), but not by Gli (0.01 mmol.L-1). The results indicated that the inhibitory effect of HCT on the contraction of rat aorta was attributable to the opening of membrane potassium channels.

Article Options

Download Citation

Cited times in Scopus