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British Journal of Pharmacology logoLink to British Journal of Pharmacology
. 1977 Jun;60(2):239–249.

The role of β-adrenoceptors in the responses of the hepatic arterial vascular bed of the dog to phenylephrine, isoprenaline, noradrenaline and adrenaline

PDI Richardson, PG Withrington
PMCID: PMC1667473  PMID: 195661

Abstract

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 β-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 β-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 β2-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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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