Hydrogen sulfide as a mediator of endothelium-dependent relaxation evoked by leaf extract in mesenteric arterial beds isolated from L-NAME hypertensive rats.

Aqueous extract of leaves (MOE) is a potent inducer of endothelium-dependent relaxation of mesenteric resistance arteries of rats induced to be hypertensive using N-nitro-L-arginine methyl ester (L-NAME). Hydrogen sulfide (HS) has been shown to participate in endothelium-dependent relaxation of small resistance arteries. Therefore, this study aimed to investigate whether endothelial HS-dependent signaling plays a role in the vasorelaxation in response to MOE.
Mesenteric arterial beds isolated from L-NAME hypertensive rats were set up in an ex vivo perfusion system for measurement of vasoreactivity. All experiments were performed in the presence of the nitric oxide synthase inhibitor, L-NAME (100 µM) and the cyclooxygenase inhibitor, indomethacin (10 µM) to prevent the formation of nitric oxide and prostanoids, respectively.
In the presence of the nitric oxide synthase inhibitor, L-NAME and the cyclooxygenase inhibitor, indomethacin, the endothelium-dependent vasorelaxation induced by MOE (0.001-3 mg) was completely inhibited by DL-propargylglycine (100 µM), which inhibits the HSgenerating enzyme, cystathionine γ-lyase. This HSdependent response was reduced by the K channel blocker; glibenclamide (10 µM), the K channel blocker; tetraethylammonium (1 µM), and the myo-endothelial gap-junctional uncoupler; 18α-glycyrrhetinic acid (10 µM). In contrast, the muscarinic receptor antagonist, atropine (100 µM), did not affect the response to MOE.
The results may suggest that HS is the likely mediator of endothelium-dependent relaxation in response to MOE in mesenteric arterial beds of L-NAME-induced hypertensive rats. MOE-induced HS-dependent vasorelaxation involves activation of K and K channels and requires myo-endothelial gap-junctional communication.

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