INCREASED α2-ADRENORECEPTOR MEDIATED VASCULAR CONTRACTION IN DIABETIC RATS

Abstract

Contractile responses of aortic ring preparations from control and diabetic rats to nonselective (noradrenaline, norepinephrine, NE) and selective .alpha.1-(phenylephrine) and .alpha.2-(clonidine) adrenoreceptor agonists were examined to determine the contribution of these receptor subtypes to the response. Aortae from diabetic rats were more responsive to NE compared to age-matched control rats. There was no difference between contractile responses of aortae from control and diabetic rats to phenylephrine, while clonidine-induced contractions were enhanced in aortae from diabetic rats. Dependence of clonidine-induced contractions on extracellular Ca availability was determined. Each of the methods used indicated increased dependency of aortae from diabetic rats on extracellular Ca availability for clonidine-induced contractile force generation. Evidently, the increase NE-induced responsiveness of aortae from diabetic rats may be attributed to an increased .alpha.2-adrenoreceptor component of the contractile response and this .alpha.2-adrenoreceptor mediated contraction is primarily dependent upon extracellular Ca. The increased contractile responsiveness of aortae from diabetic rats to .alpha.2-adrenoreceptor stimulating drugs may be related to an altered coupling mechanism between the .alpha.2-adrenoreceptors and the Ca2+ channels, or due to a change in membrane permeability as a result of the disease process.