Effects of nitric oxide (NO) on platelet-activating factor (PAF)- and. alpha. -adrenergic-stimulated vasoconstriction and glycogenolysis in the perfused rat liver

Conference · Mon Mar 11 04:00:00 EST 1991 · FASEB Journal (Federation of American Societies for Experimental Biology); (United States)

OSTI ID:5373448

Moy, J A; Bates, J N; Fisher, R A ^[1]

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1. Univ. of Iowa, Iowa City (United States)

Effects of 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 into perfused livers inhibited PAF-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 IC{sub 50} of approximately 8 {mu}M. In contrast to its effects on PAF-induced responses in the perfused liver, NO inhibited increases in hepatic portal pressure in response to phenylephrine approximately 75% without altering phenylephrine-stimulated glucose output and oxygen consumption. Similarly, infusion of NO into perfused livers inhibited significantly increases in hepatic portal pressure but not increases in glucose output in response to a submaximal concentration of phenylephrine. Like NO, sodium nitroprusside significantly inhibited hemodynamic but not glycogenolytic responses to phenylephrine in perfused livers. However, PAF-stimulated alterations in hepatic portal pressure, glucose output and oxygen consumption were unaffected by infusion of sodium nitroprusside 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.

• OSTI ID: 5373448
• Report Number(s): CONF-9104107--
• Conference Information: Journal Name: FASEB Journal (Federation of American Societies for Experimental Biology); (United States) Journal Volume: 5:4
• Country of Publication: United States
• Language: English

Related Subjects

560300* -- Chemicals Metabolism & Toxicology
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ALDEHYDES
ANIMALS
AUTONOMIC NERVOUS SYSTEM AGENTS
BIOCHEMICAL REACTION KINETICS
BIOLOGICAL EFFECTS
BLOOD COAGULATION FACTORS
BODY
CARBOHYDRATES
CHALCOGENIDES
COAGULANTS
DIGESTIVE SYSTEM
DRUGS
GLANDS
GLUCOSE
HEMATOLOGIC AGENTS
HEXOSES
INHIBITION
KINETICS
LIVER
MAMMALS
MONOSACCHARIDES
NITRIC OXIDE
NITROGEN COMPOUNDS
NITROGEN OXIDES
ORGANIC COMPOUNDS
ORGANS
OXIDES
OXYGEN COMPOUNDS
PERFUSED ORGANS
PROTEINS
RATS
REACTION KINETICS
RODENTS
SACCHARIDES
SECRETION
SYMPATHOMIMETICS
VASOCONSTRICTION
VERTEBRATES