Vascular prostacyclin release and metabolic derangement in diabetes.
Diabetic patients have a high susceptibility to microangiopathy, atherosclerosis and thrombosis. Platelet hyper-reactivity, possibly related to an imbalance in platelet/vessel wall arachidonic acid metabolism may be involved. Release of prostacyclin (PGI2) by aorta and renal cortex from diabetic rats and arteries from diabetic patients was significantly depressed. Blood glucose levels in rats at sacrifice did not correlate well with aortic PGI2 release, although in no case was a high rate of PGI2 production found in an animal with a high blood glucose level. Insulin treatment (8 days) restored PGI2 release in tissues from diabetic rats. PGI2 generation by arteries from diabetic patients taking oral hypoglycemic agents was significantly lower than that of diabetics treated with insulin. PGI2 stimulatory activity was increased in plasma from diabetic rats and patients, but diabetic rat aortas were less responsive than those of controls to diabetic plasma. This suggests that decreased values PGI2 release in diabetes is not due to lack of stimulatory plasma factors but may be due to a defect in the vessel wall. Impaired PGI2 release by tissues that develop angiopathy and its normalization in rats by insulin, suggests that depressed PGI2 production may play a role in the vascular complications of diabetes.
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000378:metabolism*; D003925:Diabetic Angiopathies / Q000188:drug therapy / Q000378:metabolism*; D011464:Epoprostenol / Q000378:metabolism*; D007328:Insulin / Q000627:therapeutic use*; D007672:Kidney Cortex / Q000378:metabolism; D008297:Male; D011453:Prostaglandins / Q000378:metabolism*; D051381:Rats
D001786:Blood Glucose; D007328:Insulin; D011453:Prostaglandins; D011464:Epoprostenol