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摘要
Apelin was recently found to be an inotropic polypeptide in isolated rat hearts, and intravenous injection of apelin can induce a transient decrease in blood pressure. To illustrate the mechanism of apelin-induced vasodilation, we observed the in vitro effects of apelin on the L-arginine (L-Arg)/nitric oxide (NO) pathway in the incubated, isolated rat aorta. Apelin stimulated vascular NO2- product and NOS activation in a concentration- and time-dependent manner. Compared with no apelin treatment, incubation with apelin (10(-9), 10(-8), and 10(-7) mol/L) increased NO2- product by 33%, 46%, and 69% (all p < 0.01), respectively, and Ca2+-dependent constitutive NOS (cNOS) activity by 200%, 460%, and 550% (all p < 0.01), respectively. However, Ca2+-independent NOS (iNOS) activity was not significantly altered (p > 0.05). Apelin incubation (10(-9), 10(-8), and 10(-7) mol/L) increased L-Arg uptake by 130%, 180%, and 240% (all p < 0.01), respectively. The mRNA level of cationic amino acid transporters, CAT-1 and CAT-2B, in rat aortic tissues treated with 10(-7) mol/L apelin was increased by 110% and 128%, respectively (both p < 0.01). Incubation with 10(-7) mol/L apelin elevated eNOS rnRNA and protein levels, by 53% (p < 0.05) and 319% (p < 0.01), respectively. Collectively, these results demonstrate that apelin directly activated the vascular L-Arg/ NOS/NO pathway, which could be one of the important mechanisms of apelin-regulated vascular function.
