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 .
C0014563
adrenaline
C0028351
noradrenaline