Endothelium-dependent relaxation in isolated renal arteries of diabetic rabbits.

Autor: Yousif, M.H.M., Cherian, A., Oriowo, M.A.
Předmět:
Zdroj: Autonomic & Autacoid Pharmacology; Apr2002, Vol. 22 Issue 2, p73-82, 10p
Abstrakt: 1 In this study, we have investigated the vasodilator response to acetylcholine under diabetes conditions in isolated renal arteries of rabbits. We have also examined the contribution of endothelium-derived nitric oxide (EDNO) and endothelium-derived hyperpolarizing factor (EDHF) to the endothelium-dependent relaxation caused by acetylcholine in the renal arteries of alloxan-induced diabetic rabbits. 2 Acetylcholine (10[sup -10]-10[sup -4] M) produced cumulative concentration-response curve in the renal arteries of both control and diabetic rabbits. The EC[sub 50] values and maximal responses to acetylcholine were not significantly different relative to diabetic conditions. In order to isolate the EDHF component of acetylcholine-induced vasodilator response, L-nitro-methyl arginine ester (L-NAME, 10[sup -4] M) and indomethacin (10[sup -6] M) were added to the Krebs' solution throughout the experiment. Under these conditions, acetylcholine induced vasodilatation in the isolated renal arteries from both control and diabetic rabbits. The vasodilator response to acetylcholine was not affected under diabetic conditions. 3 Sodium nitroprusside (SNP)-induced relaxation was increased in the diabetic rabbits compared with the control animals. 4 Tetrabutyl ammonium (TBA, 0.5 mM) produced a significant reduction in acetylcholineinduced vasodilatation in both preparations from control and diabetic animals, consistent with involvement of K[sup +] channels in mediating this response. Glibenclamide (1 µM) attenuated acetylcholine-induced vasodilatation in preparations from control animals only, while iberiotoxin (0.05 µM) significantly reduced the vasodilator response to acetylcholine in preparations from both control and diabetic animals. 5 The role of EDNa in mediating acetylcholine-induced vasodilatation was examined. The vascular preparations were incubated with 20 mM K[sup +]-Krebs' solution to inhibit the EDHF contribution to acetylcholine-induced... [ABSTRACT FROM AUTHOR]
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