Alteration of Vascular Reactivity and Regional Blood Flow in Streptozotocin-Induced Diabetic Rat
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Macro- and microvascular complications are common in diabetes mellitus and accumulating evidence has shown that insulin has a relevant effect on cardiovascular function. A vasorelaxing effect, attenuation of vasopressor response to angiotensin and epinephrine and reduction of vascular resistance have been demonstrated for insulin. In contrast, insulin is also known to stimulate sympathetic nerves, -enhance Na reabsorption in the kidney, alter Ca and Mg ion movement and increase norepinephrineinduced vasoconstriction. Insulin resistance has been linked to the development of essential hypertension. The balance between the pervioui effects markedly contributes to either the normality of BP or setting the hypertension conditions. The present study is designed to compare the regional blood flow in four different arterial resistance beds (carotid, renal, mesenteric and hindquarter vascular beds) in control versus streptozotocin induced diabetic rats (which represents a model of type I diabetes) and to investigate any possible change in the vascular reactivity of these beds to different pressor and dilator substances in the streptozotocin induced abetic rats. Blood flow in carotid, renal, mesenteric and hindquarter vascular beds was determined in normal and in streptozotocin induced diabetic rats. Vascular conductance was calculated as Flow / Pressure and DRCs of vascular conductance were constructed in the four vascular beds after the administration of the a l-drenoceptor agonist, phenypherine; the a2-drenoceptor agonist, clonidine; the p drenoceptor agonist, isoprenaline; ATII; the nitric oxide synthetase inhbitor, L-NAME and the cyclo-oxygenase inhbitor, indomethacin. The results demonstrated that in streptozotocin induced diabetic rats, regional blood flow was markedly reduced especially in the renal and hindquarters vascular beds. No change observed in the blood flow to the mesenteric bed. An enhanced response to the VC effect of clonidine, angiotensin and L-NAME was observed. No change was observed in a Idrenoceptor- mediated responses. An attenuated response to the VD effect of the isoprenaline and indomethacin was determined. Theses results suggest an impaired vascular responses in diabetes that possiblely involve endothelium, prostglandins, a2 and p adrenoreceptors.