VASODILATOR ACTION OF THE ISOPROPYL ESTER OF PALMITOYL CARNITINE IN THE RAT CORONARY CIRCULATION AND MESENTERIC VASCULAR BED

The vasodilator action of the isopropyl ester of palmitoyl carnitine (P1Pi) has been examined in perfused rat hearts and mesenteric vessels. The coronary vasodilator effect P1Pi was not significantly inhibited by flurbiprofen (10 mu M), BW755C (10 mu M), glibenclamide (10 mu M) or the bradykinin B-2 receptor antagonist D-Arg(0)[Hyp(3),Thi(5,8),D-Phe(7)]bradykinin (1 mu M), indicating that the action of P1Pi is not mediated via arachidonic acid metabolites, ATP-dependent K+ channels or bradykinin B-2 receptors. L-NG-Nitro arginine (100 mu M) did not inhibit the vasodilator action of P1Pi whilst superoxide dismutase (20 and 50 Uml(-1)) attenuated its vasodilator action. Methylene blue (10 mu M) caused inhibition in three out of four hearts, while haemoglobin (1 mu M) caused an irreversible inhibition of the action of P1Pi which was associated with a depression of myocardial contractility. In air-damaged mesenteric vascular beds the vasodilator action of P1Pi was not attenuated, whilst that of acetylcholine was abolished. In K+-depolarised mesenteric vascular beds the constrictor action of Ca2+ was attentuated by P1Pi. Therefore the vasodilator effect of P1Pi appears to be the result of a direct effect on smooth muscle.