Portal hypertension increases vasoconstrictor responsiveness of rat aorta

We have examined the effects of pre-hepatic portal hypertension on the resp onsiveness of aorta from Wistar and Sprague-Dawley rats. Rats were made por tal hypertensive by creating a calibrated portal vein stenosis, or sham ope rated. in rat aorta, there was no significant difference between portal hyp ertensive and sham-operated animals in the contractile potency of KCI, nora drenaline or phenylephrine. In aortas from Wistar rats, the maximum respons e to KCI (0.71+/-0.12 g) and noradrenaline (1.00+/-0.17 g) but not phenylep hrine (0.86+/-0.10 g) in portal hypertensive animals was significantly incr eased compared with that in sham-operated animals (0.45+/-0.04 g, 0.57+/-0. 07 g, 0.71+/-0.05 g respectively). In aortas from Sprague-Dawley rats, the maximum response to KCI (1.21+/-0.21 g) and phenylephrine (1.54+/-0.30 g) b ut not noradrenaline (0.93+/-0.09 g) in portal hypertensive animals was sig nificantly increased compared with that in sham-operated animals (0.59+/-0. 09 g, 0.76+/-0.11 g, 1.04+/-0.10 g respectively). There was no difference b etween portal hypertensive and sham-operated Wistar rats in the affinity or maximum number of binding sites for [H-3]prazosin to alpha(1)-adrenoceptor s in cardiac ventricular membranes. It is concluded that portal hypertensio n tends to produce an increase rather than a decrease in the contractile re sponse to vasoconstrictors in aorta from both Wistar and Sprague-Dawley rat s. This suggests that the diminished responsiveness to vasoconstrictors rep orted in portal hypertensive rats in vivo is not due to a diminished respon siveness at the level of the vascular smooth muscle.