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

This cross-sectional study examined responses of the isolated cystic artery to 3 alpha-adrenoceptor agonists and the effects of 2 antagonists in relation to subjects' blood pressures. Potency of the 3 amines studied 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 angiotensin II. A weak trend for increased potency of alpha-methylnorepinephrine was noted in arteries of subjects with higher blood pressures (r = 0.268, p = 0.027). There was no relationship between blood pressure and pA(2) for yohimbine. The pA(2) for prazosin could not be calculated because of a decline in maximal responses but prazosin was clearly more potent than yohimbine, The decline in maximal responses to norepinephrine and phenylephrine after prazosin treatment was related to subjects' diastolic blood pressures (r = -0.400, p = 0.003), There were no significant relationships between these measurements of vascular responsiveness and a family history of hypertension, There were also no significant relationships betwen these measurements of vascular responsiveness and plasma norepinephrine levels, alpha(2)-adrenoceptor binding or platelets of beta(2)-adrenoceptor binding of lymphocytes, The major postjunctional a-adrenoceptors in this artery are of the alpha(1) type. The data suggest that differences in potency of alpha(2)-adrenoceptor agonists in relation to blood pressure may be due to differences in the alpha(2)-adrenoceptor but are not likely due to a difference in binding to the receptor itself. The explanation for the effect of prazosin on maximal responses to alpha-adrenoceptor agonists in relationship to blood pressure in the present study requires further study, If the results in blood cell adrenoceptors are parallel to those in cystic artery, increased potency of alpha(2)-adrenoceptor agonists in the artery in subjects with higher blood pressure is not due to an increased number of adrenoceptors and therefore is most likely due to differences in postreceptor excitation-contraction coupling. Future experiments should utilize preparations such as subcutaneous resistance vessels where alpha(2)-adrenoceptors are more predominant.