Portal hypertension increases vasoconstrictor responsiveness of rat aorta.

We have examined the effects of pre-hepatic portal hypertension on the responsiveness of aorta from Wistar and Sprague-Dawley rats. Rats were made portal hypertensive by creating a calibrated portal vein stenosis, or sham operated. In rat aorta, there was no significant difference between portal hypertensive and sham-operated animals in the contractile potency of KCl, noradrenaline or phenylephrine. In aortas from Wistar rats, the maximum response to KCl (0.71+/-0.12 g) and noradrenaline (1.00+/-0.17 g) but not phenylephrine (0.86+/-0.10 g) in portal hypertensive animals was significantly increased 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 KCl (1. 21+/-0.21 g) and phenylephrine (1.54+/-0.30 g) but not noradrenaline (0.93+/-0.09 g) in portal hypertensive animals was significantly 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 between portal hypertensive and sham-operated Wistar rats in the affinity or maximum number of binding sites for [3H]prazosin to alpha1-adrenoceptors in cardiac ventricular membranes. It is concluded that portal hypertension tends to produce an increase rather than a decrease in the contractile response to vasoconstrictors in aorta from both Wistar and Sprague-Dawley rats. This suggests that the diminished responsiveness to vasoconstrictors reported in portal hypertensive rats in vivo is not due to a diminished responsiveness at the level of the vascular smooth muscle.