AI Article Synopsis
- Vascular responses to sodium arachidonate were studied in hearts from diabetic rats, revealing a biphasic response—initial vasoconstriction followed by vasodilation, unlike non-diabetic rats which only showed vasodilation.
- The vasoconstrictor phase in diabetic rats could be blocked by ONO-3708 (a thromboxane A2 antagonist) and partially inhibited by indomethacin, indicating the role of leukotrienes after cyclooxygenase inhibition.
- Additionally, the coronary response to leukotriene D4 was greater in diabetic rats, suggesting leukotrienes contribute to vascular responses in diabetes when cyclooxygenase activity is reduced.
Article Abstract
Vascular responsiveness to sodium arachidonate was examined in isolated perfused hearts from rats with streptozotocin-induced diabetes. In diabetic rats arachidonate induced a biphasic coronary vascular response characterized by initial vasoconstriction followed by prolonged vasodilation. Non-diabetic rats showed only a vasodilator response. The vasoconstrictor phase found in diabetic rats was abolished by ONO-3708, a selective thromboxane A2 antagonist. Indomethacin partly inhibited the vasoconstrictor response, the residual response being abolished by a leukotriene antagonist, ONO-1078. The vasodilator response, however, was completely abolished by indomethacin in both diabetic and nondiabetic rats. Furthermore, the coronary constrictor response to leukotriene D4 was enhanced in diabetic compared to nondiabetic rats. These results suggest an involvement of leukotriene in the vasoconstrictor response to arachidonate in diabetic rats, especially when cyclooxygenase is inhibited.
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| http://dx.doi.org/10.1007/BF00277255 | DOI Listing |
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