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

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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 α1-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 α1-adrenoceptors were determined by specific binding of [125I]-HEAT (2-β-4-hydroxy-3-iodophenyethyl-aminomethyltetralone). 3 In the presence of yohimbine (10−7 m, an α2-adrenoceptor antagonist), propranolol (10−6 m, a β-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 α1-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 α1-adrenoceptors.