Abstract
We evaluated the vasorelaxant effect of camel and bovine casein tryptic hydrolysates (CTH and BTH, respectively) and their mechanism of action in aorta and mesenteric artery of Wistar Kyoto rats. CTH produced a more potent relaxation than that induced by BTH. This relaxation was endothelium-dependent and was mediated through the activation of the nitric oxide (NO)/cyclic guanosine 3,5-monophosphate (cGMP) pathway. The intracellular level of cGMP was increased by CTH. Moreover, CTH-induced relaxation was inhibited by HOE 140, a B2 bradykinin receptors antagonist, indicating that B2 bradykinin receptors play a role in the CTH effect. In endothelium-intact mesenteric artery, CTH and BTH produced a similar concentration-dependent relaxation with a lesser maximal effect than in aortic rings. Moreover, this relaxation was inhibited by Nω nitro-l-arginine methyl ester hydrochloride, a NO synthase inhibitor, but the addition of indomethacin, a cyclooxygenase inhibitor, and tetraethylammonium, a K+ channels blocker did not potentiate the inhibition.
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