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VASCULAR BIOLOGY

Vasoconstrictive effect of hydrogen sulfide involves downregulation of cAMP in vascular smooth muscle cells

Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore

Submitted 6 April 2008 ; accepted in final form 5 September 2008

Hydrogen sulfide (H₂S), a new endogenous mediator, produces both vasorelaxation and vasoconstriction. This study was designed to examine whether cAMP mediates the vasoconstrictive effect of H₂S. We found that NaHS at a concentration range of 10–100 µM (yields 3–30 µM H₂S) concentration-dependently reversed the vasodilation caused by isoprenaline and salbutamol, two β-adrenoceptor agonists, and forskolin, a selective adenylyl cyclase activator, in phenylephrine-precontracted rat aortic rings. Pretreatment with NaHS (10–100 µM) for 5 min also significantly attenuated the vasorelaxant effect of salbutamol and forskolin. More importantly, NaHS (5–100 µM) significantly reversed forskolin-induced cAMP accumulation in vascular smooth muscle cells. However, NaHS produced significant, but weaker, vasoconstriction in the presence of N^G-nitro-L-arginine methyl ester (100 µM), a nitric oxide synthase inhibitor, or in endothelium-denuded aortic rings. Blockade of ATP-sensitive potassium channels with glibenclamide (10 µM) failed to attenuate the vasoconstriction induced by H₂S. Taken together, we demonstrated for the first time that the vasoconstrictive effect of H₂S involves the adenyly cyclase/cAMP pathway.

hydrogen sulfide; smooth muscle cell; adenosine 3',5'-cyclic monophosphate; nitric oxide; vascular contractility