Effects of beta-adrenergic stimulation on 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine-mediated vasoconstriction and glycogenolysis in the perfused rat liver

Rory A Fisher; Raj Kumar; Donald J Hanahan; Merle S Olson

doi:10.1016/S0021-9258(19)84454-X

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Effects of beta-adrenergic stimulation on 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine-mediated vasoconstriction and glycogenolysis in the perfused rat liver

Journal article

Open access

Peer reviewed

Effects of beta-adrenergic stimulation on 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine-mediated vasoconstriction and glycogenolysis in the perfused rat liver

Rory A Fisher, Raj Kumar, Donald J Hanahan and Merle S Olson

The Journal of biological chemistry, Vol.261(19), pp.8817-8823

07/05/1986

DOI: 10.1016/S0021-9258(19)84454-X

PMID: 3013865

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Abstract

The beta-adrenergic agonist isoproterenol inhibited the glycogenolytic response of platelet-activating factor (AGEPC, 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine) in perfused livers derived from fed rats. AGEPC-stimulated hepatic vasoconstriction, measured by increases in portal vein pressure, also was inhibited by prior isoproterenol infusion. Isoproterenol-mediated inhibition of these hepatic responses to AGEPC was not apparent when isoproterenol (10 microM) was coinfused with the beta-receptor antagonist propranolol (75 microM) or when isoproterenol was replaced with the alpha-adrenergic agonist phenylephrine (10 microM). alpha-Agonist-induced glycogenolysis and vasoconstriction in the perfused liver was unaffected by isoproterenol infusion. Glucagon (2.3 nM) had no effect on the glycogenolytic or vasoconstrictive responses of the liver to AGEPC despite the fact that glucagon increased hepatic cAMP levels to a far greater extent than isoproterenol. Additionally, inhibition of the hepatic responses to AGEPC by isoproterenol occurred in perfused livers from mature rats (i.e. greater than 300 g) in which liver parenchymal cells lack functional beta-adrenergic receptors. The data presented in this study illustrate a specific inhibition of AGEPC-induced hepatic glycogenolysis and vasoconstriction by beta-adrenergic stimulation of the perfused liver. This inhibition appears to be mediated by interaction of isoproterenol with nonparenchymal cells within the liver. These findings are consistent with the concept that AGEPC stimulates hepatic glycogenolysis by an indirect mechanism involving hepatic vasoconstriction.

Liver - metabolism

Platelet Activating Factor - pharmacology

Rats

Male

Rats, Inbred Strains

Vasoconstriction - drug effects

Propranolol - pharmacology

Animals

Liver Glycogen - metabolism

Phenylephrine - pharmacology

Liver - drug effects

Liver Circulation - drug effects

Perfusion

Isoproterenol - pharmacology

Kinetics

Receptors, Adrenergic, beta - drug effects

Details

Title: Subtitle: Effects of beta-adrenergic stimulation on 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine-mediated vasoconstriction and glycogenolysis in the perfused rat liver
Creators: Rory A Fisher
Raj Kumar
Donald J Hanahan
Merle S Olson
Resource Type: Journal article
Publication Details: The Journal of biological chemistry, Vol.261(19), pp.8817-8823
DOI: 10.1016/S0021-9258(19)84454-X
PMID: 3013865
NLM abbreviation: J Biol Chem
ISSN: 0021-9258
eISSN: 1083-351X
Publisher: United States
Grant note: AM-07358 / NIADDK NIH HHS AM-33538 / NIADDK NIH HHS
Language: English
Date published: 07/05/1986
Academic Unit: Iowa Neuroscience Institute; Neuroscience and Pharmacology; Internal Medicine
Record Identifier: 9984040329602771

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