Aortic vascular and atrial responses to (+/-)-1-O-octadecyl-2-acetyl-glyceryl-3-phosphorylcholine.
The effects of (+/-)-1-O-octadecyl-2-acetyl-glyceryl-3-phosphorylcholine (octadecyl-AGPC) were studied in three types of aortic vascular smooth muscle preparations, namely, strips, rubbed and unrubbed rings, and an atrial preparation in normotensive rats. In the resting tension state, octadecyl-AGPC did not elicit significant contractions in either rubbed or unrubbed ring preparations at concentrations lower than 1 X 10(-4) M. However, at a concentration of 3 X 10(-4) M, octadecyl-AGPC markedly contracted both types of ring preparations. This contractile response was partially antagonized by pretreatment with reserpine and completely blocked by phentolamine (1 X 10(-6) M). In preparations contracted with noradrenaline (NA), octadecyl-AGPC elicited biphasic responses in intact ring preparations; an initial relaxation followed by contraction. Octadecyl-AGPC induced only a slight contraction in strips and a slight relaxation in the rubbed ring preparation. Octadecyl-AGPC did not elicit any significant effect on chronotropy or inotropy at concentrations up to 3 X 10(-5) M. When the concentration was 1 X 10(-4) M, octadecyl-AGPC produced significant positive chronotropic and inotropic effects on spontaneously beating right and electrically driven left atrial preparations, respectively. Both effects were blocked by propranolol (5 X 10(-8) M); reserpine pretreatment antagonized only the chronotropic response. In [3H]-dihydroalprenolol [( 3H]-DHA) binding studies, octadecyl-AGPC had a Kd of 427.85 microM and thus was much less potent than isoprenaline (Kd = 465.10 nM) or propranolol (Kd = 4.4 nM) in displacing [3H]-DHA in rat cardiac membrane preparations. 6 In conclusion, relaxation and contraction induced by octadecyl-AGPC in aortic preparations is an indirect rather than a direct effect. An unknown factor released from endothelial cells is responsible for aortic smooth muscle relaxation by octadecyl-AGPC while released NA appears to be responsible for aortic vascular contraction and for the positive chronotropic and inotropic effects in the atrial preparations.
D000818:Animals; D001011:Aorta / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006325:Heart Atria / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009200:Myocardial Contraction / Q000187:drug effects; D010972:Platelet Activating Factor / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013268:Stimulation, Chemical
D010972:Platelet Activating Factor; C026613:1-0-octadecyl 2-0-acetyl sn-glycero-3-phosphorylcholine