Role of GABA[B] receptor and L-Arg in GABA induced vasorelaxation in non-diabetic and streptozotocin- induced diabetic rat vessels

Hypertension is considered an independent risk factor for cardiovascular mortality in diabetic patients. The present study was designed to determine the role of gamma amino butyric acid B [GABA[B]] receptor and L-arginine [L-Arg] in GABA-induced vasorelaxation in normal and streptozotocin-induced diabetic rat vessels. Diabetes was induced by a single i.p. injection of streptozotocin [STZ, 60 mg/kg]. Eight weeks later, superior mesenteric arteries of all groups were isolated and perfused according to the McGregor method. Baseline perfusion pressure of STZ diabetic rats was significantly higher than non-diabetic rats in both intact and denuded endothelium. In the presence of faclofen, a selective GABA[B] receptor blocker, GABA-induced relaxation in intact and denuded endothelium mesenteric beds of STZ diabetic rats was suppressed, but this response in nondiabetic rats was not suppressed. Our results showed that in the presence of L-Arg, a nitric oxide precursor, GABA induced vasorelaxation in both diabetic and non-diabetic vessels. From the results of this study, it may be concluded that the vasorelaxatory effect of GABA in diabetic vessel is mediated by the GABA[B] receptor and nitric oxide, but it seems that in non-diabetic vessel GABA[B] receptor does not play any role in GABA-induced vasorelaxation, but nitric oxide induced GABA relaxation in non-diabetic vessel

Relaxatory effect of gamma-aminobutyric acid [GABA] is mediated by same pathway in diabetic and normal rat mesenteric bed vessel

Diabetes related dysfunction of resistance vessels is associated with vascular occlusive diseases. Vasorelaxant agents may have a role in control of diabetic cardiovascular complications. Gamma aminobutyric acid [GABA] has demonstrated to cause vasorelaxation. The present study was designed to determine i] the vasorelaxatory effect of GABA on diabetic vessels and ii] the role of endothelium in GABA-induced vasorelaxation. After Diabetes induction,. Mesenteric arteries of animals were perfused. Vascular beds were constricted with phenylephrine. GABA [1 to 50 micro M] was added into the medium and perfusion pressure was then recorded. In all groups of animals, relaxant response to GABA in mesenteric bed appeared. Although diabetes induction did not change mesenteric bed response to GABA, denuded vessels showed a reduced response to GABA both in control and diabetic animals. GABA can induce endothelium dependent vasorelaxation in mesenteric vessels in normal and diabetic rats