STUDY ON THE VASCULAR REACTIVITY AND ALPHA(1)-ADRENOCEPTORS OF PORTAL HYPERTENSIVE RATS

1 Vascular hyporesponsiveness in portal hypertension has been demonstrated to various vasoconstrictors including noradrenaline (NA). The present study aimed to determine whether the attenuated vascular responsiveness to NA is due to a change in the affinity or the number of alpha(1)-adrenoceptors. 2 Partial portal vein ligation (PVL) was performed in Sprague-Dawley rats to produce portal hypertension. Vascular responsiveness to NA was assayed in portal vein, mesenteric artery or tail artery. The affinity and number of alpha(1)-adrenoceptors were determined by specific binding of [I-125]-HEAT (2-beta-4-hydroxy-3-iodophenyethyl-aminomethyltetralone). 3 In the presence of yohimbine (10(-7) M, an alpha(2)-adrenoceptor antagonist), propranolol (10(-6) M, beta-adrenoceptor antagonist), and two catecholamine uptake inhibitors, desipramine (10(-7) M) and normetanephrine (10(-6) M), the maximum responses to NA were decreased in all three blood vessels of PVL rats: 45% decrease in portal vein, 25% in mesenteric artery and 18% in tail artery. 4 The EC(50) values of NA and the pA(2) values of prazosin, an alpha(1)-adrenoceptor antagonist, in all three blood vessels were not significantly different between sham-operated and PVL rats. 5 The K-D and B-max values for specific binding of [I-125]-HEAT or the K-1 values for NA in the crude membrane preparations of either mesenteric artery or tail artery were also not significantly different between the two groups. 6 It is concluded that the vascular hyporesponsiveness to NA in the mesenteric artery or tail artery of PVL rats is not due to changes in the affinity or number of alpha(1)-adrenoceptors.