The role of beta-adrenoceptors in the responses of the hepatic arterial vascular bed of the dog to phenylephrine, isoprenaline, noradrenaline and adrenaline.
1 The sympathetically-innervated hepatic arterial vascular bed of the dog was perfused from a femoral artery. Hepatic arterial blood flow and perfusion pressure were recorded continuously, and the hepatic arterial vascular resistance (HAVR) calculated from these measurements.2 Intra-arterial injections of phenylephrine caused dose-dependent rises in HAVR, indicating hepatic arterial vasoconstriction, at all doses above threshold. No secondary reductions in HAVR followed these responses.3 Intra-arterial injections of isoprenaline caused only dose-dependent reductions in HAVR at doses above threshold.4 Intra-arterial injections of noradrenaline typically caused an initial increase in HAVR which was followed at all but the highest doses by a secondary, delayed, reduction in HAVR.5 Intra-arterial injections of adrenaline, like those of noradrenaline, resulted in hepatic arterial vasoconstriction followed by hepatic arterial vasodilatation.6 On a molar basis, the most potent hepatic arterial vasoconstrictor was noradrenaline, followed by adrenaline and phenylephrine.7 The maximum reductions in HAVR caused by adrenaline (mean reduction = 21.9%) and noradrenaline (16.9%) were significantly smaller than those due to isoprenaline ((P) < 0.001).8 Propranolol attenuated the hepatic arterial vasodilator responses due to isoprenaline, and the secondary falls in HAVR following intra-arterial adrenaline and noradrenaline.9 Propranolol did not modify the vasoconstrictor responses to phenylephrine.10 Both adrenaline and noradrenaline were more potent hepatic arterial vasoconstrictors after propranolol than in the absence of beta-adrenoceptor blockade. The potentiation of the vasoconstrictor effects of adrenaline was statistically significant.11 After propranolol, adrenaline was a more potent hepatic arterial vasoconstrictor than noradrenaline.12 Since the beta-adrenoceptors in the hepatic arterial vasculature were not blocked by atenolol, but were stimulated by salbutamol, it is concluded that they are predominantly of the beta(2)-type.13 The vasoconstrictor actions of phenylephrine, noradrenaline and adrenaline were all antagonized by the systemic administration of phentolamine, all three dose-response curves being shifted to the right.14 The results are discussed with regard to the possible control of the hepatic arterial vasculature by naturally-occurring catecholamines.
D000420:Albuterol / Q000494:pharmacology; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004837:Epinephrine / Q000494:pharmacology*; D006499:Hepatic Artery / Q000294:innervation; D007545:Isoproterenol / Q000494:pharmacology*; D008102:Liver Circulation / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology*; D010656:Phenylephrine / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D014655:Vascular Resistance / Q000187:drug effects
D011941:Receptors, Adrenergic; D011943:Receptors, Adrenergic, beta; D010656:Phenylephrine; D001262:Atenolol; D011433:Propranolol; D007545:Isoproterenol; D000420:Albuterol; D009638:Norepinephrine; D004837:Epinephrine