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

effect of [teucrium polium l.] extracts on insulin release from in situ isolated perfused rat pancreas in a newly modified isolation method: the role of ca[2+] and k[+] channels

[Teucrium polium L] [TP] has been long recommended in Iranian folk medicine for its anti-diabetic activities. We attempt here to evaluate the effect of TP extract on insulin secretion in rat pancreas. Rat pancreas was isolated in situ and perfused with Krebs solution containing low glucose [LG, 2.8 mM] or high glucose [HG, 16.7 mM] as perfusate. The aqueous extract [Aq. E] and methanolic extract [Met. E] of TP aerial parts and two partition fractions of Met. E were added to perfusate to evaluate insulin release. Diazoxide [DZX] and verapamil [VPM] were also used for assessing the probable mechanism of the effects. In each experimental group, the peak and baseline of insulin levels in effluent samples were compared. The GC/MS analysis was carried out to detect active ingredients in the extracts. Adding Met. E to the LG caused a significant increase [P<0.05] in insulin release from the basal level of 0.17 +/- 0.05 micro g/1 to a peak value of 3.94 +/- 1.29 micro g/1, when Met. E was introduced to the HG, there was a further protracted stimulation of insulin release from 2.15 +/- 1.35 micro g/1 to 6.16 +/- 0.52 micro g/1. Both DZX and VPM when added separately to the LG, led to inhibition of Met. E induced insulin secretion. The Aq. E and fractions had no significant effect on insulin secretion. Only in the Met. E, the component 5-hydroxy-4.7-dimethoxyflavone [apigenin-4,7-dimethylether] was detected. It can be concluded that the insulinotropic properties of TP extracts can be attributed to the presence of apigenin existing only in Met. E, but not in Aq. E and fractions. Moreover, certain types of K[+] and Ca[2+] channels take part in this effect