Endothelium-dependent vasorelaxation induced by L-carnitine in isolated aorta from normotensive and hypertensive rats

The aim of this work was to investigate the mechanism of the vasodilatory effect induced by L-carnitine. Relaxation produced by L-carnitine was studied in rat aortic rings with and without functional endothelium, pre-contracted with phenylephrine by adding cumulative doses of L-carnitine (10(-7) to 10(-3) M). The relaxation evoked by L-carnitine reached higher values in aortic rings from spontaneously hypertensive rats than those obtained in arteries from normotensive rats; no relaxation was produced in de-endothelialized arteries. However, in the presence of N-G-nitro-L-arginine (3 x 10(-5) M, a nitric oxide synthase inhibitor), Ro 68070 (10(-4) M, a thromboxane synthetase inhibitor-thromboxane A(2)/prostaglandin H-2 receptor antagonist) or ICI 192605(10(-5) M, a thromboxane A(2) receptor antagonist) the relaxant response to L-carnitine was significantly inhibited. These results show that L-carnitine induced endothelium-dependent relaxation in the rat aorta and the mechanism of this relaxation appeared to be mostly mediated by endothelial production of nitric oxide but also could involve prevention of the action of cyclooxygenase endothelial products acting on the thromboxane A(2)/prostagland in H-2 receptor.