Effects of nitric oxide on platelet-activating factor- and alpha-adrenergic-stimulated vasoconstriction and glycogenolysis in the perfused rat liver

Jadine A Moy; James N Bates; Rory A Fisher

doi:10.1016/S0021-9258(18)92945-5

Back

Effects of nitric oxide on platelet-activating factor- and alpha-adrenergic-stimulated vasoconstriction and glycogenolysis in the perfused rat liver

Journal article

Open access

Peer reviewed

Effects of nitric oxide on platelet-activating factor- and alpha-adrenergic-stimulated vasoconstriction and glycogenolysis in the perfused rat liver

Jadine A Moy, James N Bates and Rory A Fisher

The Journal of biological chemistry, Vol.266(13), pp.8092-8096

05/05/1991

DOI: 10.1016/S0021-9258(18)92945-5

PMID: 1673678

Files and links (1)

url

https://doi.org/10.1016/S0021-9258(18)92945-5View

Published (Version of record) Open Access

Abstract

Effects of nitric oxide (NO) on hemodynamic and glycogenolytic responses to platelet-activating factor (PAF) and phenylephrine were investigated in perfused livers derived from fed rats. Infusion of NO (34 microM) into perfused livers inhibited PAF (0.22 nM)-induced increases in hepatic glucose output and portal pressure approximately 90 and 85%, respectively, and abolished effects of PAF on hepatic oxygen consumption. NO attenuated PAF-stimulated increases in glucose output and portal pressure, the latter indicative of hepatic vasoconstriction, with a similar dose dependence with an IC50 of approximately 8 microM. In contrast to its effects on PAF-induced responses in the perfused liver, NO inhibited increases in hepatic portal pressure in response to phenylephrine (10 microM) approximately 75% without altering phenylephrine-stimulated glucose output and oxygen consumption. Similarly, infusion of NO into perfused livers significantly inhibited increases in hepatic portal pressure but not in glucose output in response to a submaximal concentration of phenylephrine (0.4 microM). Like NO, sodium nitroprusside (83 microM) significantly inhibited hemodynamic but not glycogenolytic responses to phenylephrine in perfused livers. However, PAF (0.22 nM)-stimulated alterations in hepatic portal pressure, glucose output, and oxygen consumption were unaffected by infusion of sodium nitroprusside (83 microM) into perfused livers. These results provide the first evidence for regulatory effects of NO in the perfused liver and support the contention that PAF, unlike phenylephrine, stimulates glycogenolysis by mechanisms secondary to hepatic vasoconstriction. These observations raise the intriguing possibility that NO may act in liver to regulate hemodynamic responses to vasoactive mediators.

Hemodynamics

Receptors, Adrenergic, alpha - metabolism

Culture Techniques

Nitric Oxide - pharmacology

Liver - metabolism

Oxygen Consumption

Vasoconstriction

Rats

Male

Adrenergic alpha-Antagonists - pharmacology

Nitroprusside - pharmacology

Rats, Inbred Strains

Platelet Activating Factor - metabolism

Animals

Glycogen - metabolism

Phenylephrine - pharmacology

Perfusion

Liver - physiology

Details

Title: Subtitle: Effects of nitric oxide on platelet-activating factor- and alpha-adrenergic-stimulated vasoconstriction and glycogenolysis in the perfused rat liver
Creators: Jadine A Moy - Department of Pharmacology, University of Iowa, College of Medicine, Iowa City 52242
James N Bates
Rory A Fisher
Resource Type: Journal article
Publication Details: The Journal of biological chemistry, Vol.266(13), pp.8092-8096
DOI: 10.1016/S0021-9258(18)92945-5
PMID: 1673678
NLM abbreviation: J Biol Chem
ISSN: 0021-9258
eISSN: 1083-351X
Publisher: United States
Grant note: HL-41071 / NHLBI NIH HHS DK-25295 / NIDDK NIH HHS
Language: English
Date published: 05/05/1991
Academic Unit: Iowa Neuroscience Institute; Anesthesia; Neuroscience and Pharmacology; Internal Medicine
Record Identifier: 9984006436102771

Metrics

25 Record Views

35 Times Cited - Web of Science