Inhibition of Ras-GTPase improves diabetes-induced abnormal vascular reactivity in the rat perfused mesenteric vascular bed.

Objective: The signalling mechanisms involved in regulating altered vascular reactivity in diabetes are not fully understood. The aim of this study was to investigate the role of Ras-GTPase in the development of abnormal vascular reactivity in diabetes.

Materials And Methods: We investigated the ability of chronic administration of FPTIII (1.

Histamine-induced vasodilatation in the perfused mesenteric arterial bed of diabetic rats.

In this study, we have examined the contribution of endothelium-derived nitric oxide (EDNO) and endothelium-derived hyperpolarizing factor (EDHF) to histamine-induced endothelium-dependent relaxation in the perfused mesenteric arterial bed of rats treated with streptozotocin (STZ) to induce diabetes. Histamine (10(-10) to 5 x 10(-6) mol) produced dose-dependent vasodilator response in the perfused mesenteric arterial bed of both control and diabetic animals. In order to isolate the EDHF component of histamine-induced vasodilator response, NG-nitro-L-arginine-methyl ester hydrochloride (L-NAME) (10(-4) M) and indomethacin (10(-6) M) were added to the Krebs solution throughout the experiment.

Diabetes differentially modulated receptor- and non-receptor-mediated relaxation in rat renal artery.

In this study, we have investigated the vasodilator response to acetylcholine under diabetic conditions in isolated renal arteries of Wistar rats. The effect of nitric oxide synthase (NOS) inhibition on acetylcholine-induced vasodilator response was investigated. We have also examined the effects of two endothelium-dependent agonists which induce receptor-dependent and receptor-independent vasodilator responses.

BRL 37344 inhibited adrenergic transmission in the rat portal vein via atypical beta-adrenoceptors.

The effect of BRL 37344, a beta(3)-adrenergic agonist on adrenergic transmission in isolated segments of the rat portal vein was examined in this study. BRL 37344 (10(-9) - 10(-5)M) produced concentration-dependent inhibition of electrically induced contractions. This inhibitory effect of BRL 37344 was not antagonized by propranolol ( 10(-6)M).