title: Portal hypertension increases vasoconstrictor responsiveness of rat aorta.
abstract: 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.
authors.affiliation: Department of Physiology, Royal College of Surgeons in Ireland, Dublin 2, Ireland.
authors.forename: C
authors.initials: C
authors.lastname: Connolly
authors.forename: T
authors.initials: T
authors.lastname: Cawley
authors.forename: P A
authors.initials: PA
authors.lastname: McCormick
authors.forename: J R
authors.initials: JR
authors.lastname: Docherty
mesh_terms: D000818:Animals; D001011:Aorta; D001665:Binding Sites; D006352:Heart Ventricles / Q000378:metabolism; D006975:Hypertension, Portal / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D017082:Portal Pressure; D011189:Potassium Chloride / Q000494:pharmacology; D011224:Prazosin / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D011189:Potassium Chloride; D009638:Norepinephrine; D011224:Prazosin