Study on the vascular reactivity and α1‐adrenoceptors of portal hypertensive rats

Abstract

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 [125I]-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, a 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 EC50 values of NA and the pA2 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 KD and Bmax values for specific binding of [125I]-HEAT or the Ki 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.