PROSTACYCLIN RELEASE IN EXPERIMENTAL DIABETES - EFFECTS OF EVENING PRIMROSE OIL

Alterations in release of endothelium-derived vasomotor agents could u nderlie microvascular and neuropathic complications in diabetes. This study examined release of the potent vasodilator prostacyclin, measure d as immunoreactive 6-keto prostaglandin F-1 alpha from rat lung, kidn ey and peripheral nerve. Tissues were taken from control and streptozo tocin-diabetic rats which had been treated for 8 weeks with either eve ning primrose oil (EPO) or, as a control for lipid intake, coconut oil (CO). Lung and kidney slices were incubated in the presence of acetyl choline (ACh), the calcium ionophore 4-Br-A23187, arachidonic acid (AA ) or without agonist (basal). Segments of sciatic nerve, with their ep ineuria punctured, were incubated with or without 4-Br-A23187. Basal p rostacyclin release from the lung was significantly higher in rats tre ated with EPO irrespective of diabetic state (increased by 60% in cont rols and by 77% in diabetics). Levels were reduced in CO-diabetics com pared to EPO-controls (53% reduction) and CO-controls (30% reduction), although this did not reach statistical significance in the latter. n asal prostacyclin release was also significantly reduced in the kidney from CO-diabetics (40% reduction compared to CO-controls and 56% redu ction compared to EPO-controls). In the presence of AA, lung prostacyc lin release was significantly lower in CO-diabetic rats compared to al l other groups (40% reduction compared to EPO-diabetics and 60% compar ed to both control groups) but there were no differences in renal rele ase between any group, Prostacyclin release by nerves from CO-diabetic rats was significantly reduced (by 91-93%) compared to all other grou ps. Under ACh- and 4-Br-A23187-stimulated conditions release from any tissue did not differ significantly from basal. These data thus indica te reduced prostacyclin release from diabetic lung, kidney and nerve, which may be due in part to reduced cyclooxygenase activity. Deficits in release were attenuated, if not prevented, by treatment with EPO. T his may further suggest a decreased availability of AA for prostacycli n production in diabetes.