Transfer of arachidonate from phosphatidylcholine to phosphatidylethanolamine and triacylglycerol in guinea pig alveolar macrophages.

Guinea pig alveolar macrophages were labeled by incubation with either arachidonate or linoleate. Arachidonate labeled phosphatidylcholine (PC), phosphatidylethanolamine (PE) and triglycerides (TG) equally well, with each lipid containing about 30% of total cellular radioactivity. In comparison to arachidonate, linoleate was recovered significantly less in PE (7%) and more in TG (47%). To investigate whether redistributions of acyl chains among lipid classes took place, the macrophages were incubated with 1-acyl-2-[1-14C]arachidonoyl PC or 1-acyl-2-[1-14C]linoleoyl PC. After harvesting, the cells incubated with 1-acyl-2-[1-14C]linoleoyl PC contained 86% of the recovered cellular radioactivity in PC, with only small amounts of label being transferred to PE and TG (3 and 6%, respectively). More extensive redistributions were observed with arachidonate-labeled PC. In this case, only 60% of cellular radioactivity was still associated with PC, while 22 and 12%, respectively, had been transferred to PE and TG. Arachidonate transfer from PC to PE was unaffected by an excess of free arachidonate which inhibited this transfer to TG for over 90%, indicating that different mechanisms or arachidonoyl CoA pools were involved in the transfer of arachidonate from PC to PE and TG. Cells prelabeled with 1-acyl-2-[1-14C]arachidonoyl PC released 14C-label into the medium upon further incubation. This release was slightly stimulated by zymosan and threefold higher in the presence of the Ca2+-ionophore A23187. Labeling of macrophages with intact phospholipid molecules appears to be a suitable method for studying acyl chain redistribution and release reactions.

The cardiovascular effects of propranolol in adrenalectomized spontaneously hypertensive rats and the opposing influence of rauwolscine.

In conscious adrenalectomized spontaneously hypertensive rats (SHR) propranolol (5 mg/kg s.c.) induced an acute and profound decrease in blood pressure and heart rate, the maximum effect occurring 15-30 min after propranolol administration. The decrease was associated with a fall in cardiac output. Rauwolscine pretreatment abolished the propranolol-induced hypotension but not the bradycardia. The fall in cardiac output was significantly reduced. These results suggest that in adrenalectomized SHR the hypotensive effect of propranolol is due to the modulation of catecholamine release from nerve terminals.