Journal article
β2-Adrenergic agonist regulation of immune aggregate- and platelet-activating factor-stimulated hepatic metabolism
The Journal of biological chemistry, Vol.264(19), pp.10976-10981
07/05/1989
DOI: 10.1016/S0021-9258(18)60414-4
PMID: 2544577
Abstract
Vasoconstriction and subsequent glycogenolysis stimulated by immune complex infusion into perfused rat livers was inhibited by prior infusion of isoproterenol. Similarly, isoproterenol inhibited the biosynthesis of bioactive lipid autacoids such as platelet-activating factor, prostaglandin E2, and thromboxane B2 which was stimulated by immune aggregates. The adrenergic receptor specificity of these effects was determined through the use of specific adrenergic subtype-specific agonists and antagonists to be mediated by beta 2-adrenergic receptors. Indirect evidence for the differential expression of hepatic sinusoidal and parenchymal beta-adrenergic receptors in the male rat during ontogeny suggested that inhibition of immune aggregate-stimulated autacoid biosynthesis, vasoconstriction, and glycogenolysis by isoproterenol occurs at a sinusoidal locus, most likely Kupffer cells. In contrast with the ability of beta 2-adrenergic agonists to inhibit immune aggregate- and platelet-activating factor-stimulated hepatic metabolism, dibutyryl cyclic AMP did not mimic these sinusoidal beta 2-adrenergic effects, despite stimulating hepatic parenchymal cell glycogenolysis as effectively as isoproterenol. These observations suggest a role for cyclic AMP-independent mechanisms in the regulation of heterologous stimulus-response coupling by hepatic sinusoidal beta 2-adrenergic receptors.
Details
- Title: Subtitle
- β2-Adrenergic agonist regulation of immune aggregate- and platelet-activating factor-stimulated hepatic metabolism
- Creators
- Mark E Steinhelper - Department of Biochemistry, University of Texas Health Science Center, San Antonio 78284-7760Rory A FisherG E RevtyakDonald J HanahanM S Olson
- Resource Type
- Journal article
- Publication Details
- The Journal of biological chemistry, Vol.264(19), pp.10976-10981
- DOI
- 10.1016/S0021-9258(18)60414-4
- PMID
- 2544577
- NLM abbreviation
- J Biol Chem
- ISSN
- 0021-9258
- eISSN
- 1083-351X
- Publisher
- United States
- Grant note
- DK-19473 / NIDDK NIH HHS AM-07358 / NIADDK NIH HHS DK-33538 / NIDDK NIH HHS
- Language
- English
- Date published
- 07/05/1989
- Academic Unit
- Iowa Neuroscience Institute; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040206602771
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