ALPHA-ADRENOCEPTOR RESPONSES OF AN ISOLATED HUMAN ARTERY AND BLOOD-PRESSURE

This cross-sectional study examined responses of the isolated cystic a rtery to 3 alpha-adrenoceptor agonists and the effects of 2 antagonist s in relation to subjects' blood pressures. Potency of the 3 amines st udied was: alpha-methylnorepinephrine > norepinephrine > phenylephrine . Responses to clonidine were trivial (< 5% of maximum) and remained < 25% of maximum in the presence of subthreshold concentrations of angi otensin II. A weak trend for increased potency of alpha-methylnorepine phrine was noted in arteries of subjects with higher blood pressures ( r = 0.268, p = 0.027). There was no relationship between blood pressur e and pA(2) for yohimbine. The pA(2) for prazosin could not be calcula ted because of a decline in maximal responses but prazosin was clearly more potent than yohimbine, The decline in maximal responses to norep inephrine and phenylephrine after prazosin treatment was related to su bjects' diastolic blood pressures (r = -0.400, p = 0.003), There were no significant relationships between these measurements of vascular re sponsiveness and a family history of hypertension, There were also no significant relationships betwen these measurements of vascular respon siveness and plasma norepinephrine levels, alpha(2)-adrenoceptor bindi ng or platelets of beta(2)-adrenoceptor binding of lymphocytes, The ma jor postjunctional a-adrenoceptors in this artery are of the alpha(1) type. The data suggest that differences in potency of alpha(2)-adrenoc eptor agonists in relation to blood pressure may be due to differences in the alpha(2)-adrenoceptor but are not likely due to a difference i n binding to the receptor itself. The explanation for the effect of pr azosin on maximal responses to alpha-adrenoceptor agonists in relation ship to blood pressure in the present study requires further study, If the results in blood cell adrenoceptors are parallel to those in cyst ic artery, increased potency of alpha(2)-adrenoceptor agonists in the artery in subjects with higher blood pressure is not due to an increas ed number of adrenoceptors and therefore is most likely due to differe nces in postreceptor excitation-contraction coupling. Future experimen ts should utilize preparations such as subcutaneous resistance vessels where alpha(2)-adrenoceptors are more predominant.