Increased alpha 2-adrenoreceptor mediated vascular contraction in diabetic rats.

Contractile responses of aortic ring preparations from control and diabetic rats to nonselective (noradrenaline) 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 noradrenaline compared to age-matched control rats. There was no difference between contractile responses of aortae from control and diabetic rats to phenylephrine, whereas clonidine-induced contractions were enhanced in aortae from diabetic rats. Dependence of clonidine-induced contractions on extracellular calcium availability was determined. Each of the methods used indicated increased dependency of aortae from diabetic rats on extracellular calcium availability for clonidine-induced contractile force generation. These data indicate that the increased noradrenaline-induced responsiveness of aortae from diabetic rats may be attributed to an increased alpha 2-adrenoreceptor component of the contractile response. It is also concluded that the alpha 2-adrenoreceptor mediated contraction is primarily dependent upon extracellular calcium. From this we suggest that 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 calcium ion channels or due to a change in membrane permeability as a result of the disease process.