Criddle D N, Rad-Niknam M, Dewar G H, Woodward B
Department of Pharmacy and Pharmacology, University of Bath, Avon, UK.
Eur J Pharmacol. 1994 Apr 1;255(1-3):223-8. doi: 10.1016/0014-2999(94)90101-5.
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 microM), BW755C (10 microM), glibenclamide (10 microM) or the bradykinin B2 receptor antagonist D-Arg0[Hyp3,Thi5,8,D-Phe7]bradykinin (1 microM), indicating that the action of P1Pi is not mediated via arachidonic acid metabolites, ATP-dependent K+ channels or bradykinin B2 receptors. L-NG-Nitro arginine (100 microM) did not inhibit the vasodilator action of P1Pi whilst superoxide dismutase (20 and 50 U.ml-1) attenuated its vasodilator action. Methylene blue (10 microM) caused inhibition in three out of four hearts, while haemoglobin (1 microM) 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 attenuated by P1Pi. Therefore the vasodilator effect of P1Pi appears to be the result of a direct effect on smooth muscle.
已在灌注大鼠心脏和肠系膜血管中研究了棕榈酰肉碱异丙酯（P1Pi）的血管舒张作用。氟比洛芬（10微摩尔）、BW755C（10微摩尔）、格列本脲（10微摩尔）或缓激肽B2受体拮抗剂D-Arg0[Hyp3,Thi5,8,D-Phe7]缓激肽（1微摩尔）对P1Pi的冠状动脉舒张作用无显著抑制，这表明P1Pi的作用不是通过花生四烯酸代谢产物、ATP依赖性钾通道或缓激肽B2受体介导的。L-NG-硝基精氨酸（100微摩尔）不抑制P1Pi的血管舒张作用，而超氧化物歧化酶（20和50单位/毫升）减弱其血管舒张作用。亚甲蓝（10微摩尔）在四分之三的心脏中引起抑制，而血红蛋白（1微摩尔）对P1Pi的作用产生不可逆抑制，这与心肌收缩力降低有关。在空气损伤的肠系膜血管床中，P1Pi的血管舒张作用未减弱，而乙酰胆碱的血管舒张作用则被消除。在钾离子去极化的肠系膜血管床中，P1Pi减弱了钙离子的收缩作用。因此，P1Pi的血管舒张作用似乎是对平滑肌直接作用的结果。
