| Portal vascular responsiveness to sympathetic stimulation and nitric oxide in cirrhotic rats. | |
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MedLine Citation:
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PMID: 8836907 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS/METHODS: The modulatory role of nitric oxide in portal vasoconstrictor responses was investigated in the isolated perfused liver of cirrhotic rats (induced by carbon tetrachloride/phenobarbitone; n = 6). Age-matched (n = 5) and phenobarbitone-treated rats (n = 5) served as controls. RESULTS: At a constant flow rate of 5 ml/min there was no difference in basal perfusion pressure between the groups. Responses to electrical field stimulation of perivascular nerves caused frequency-dependent increases in perfusion pressure that were not significantly different between the groups. In contrast, dose-dependent vasoconstrictor responses to bolus injections of noradrenaline were up to two-fold greater than those observed in controls (p < 0.05). Vasoconstrictor responses to bolus injections of methoxamine (a selective alpha 1-adrenoceptor agonist) or adenosine 5'-triphosphate (ATP, a cotransmitter with noradrenaline in sympathetic nerves) were dose-dependent and similar between the groups. Infusion of the nitric oxide synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 30 microM) had no effect on basal tone or on responses to electrical field stimulation or injected agents. A step-wise increase in flow to 10, 15 and 20 ml/min produced a similar increase in perfusion pressure within each group. At increased flow, there was a decrease in responsiveness to noradrenaline (5 nmol) in preparations from all groups. In the presence of the K+ channel inhibitor glibenclamide (5 microM), the effect of noradrenaline in the cirrhotic group at flow rates of 5, 10 and 15 ml/min was maintained to a significantly greater extent than in either control group, suggesting that ATP-sensitive K+ channels in the portal venous bed may be activated in cirrhosis. CONCLUSIONS: We conclude that portal vasoconstriction associated with noradrenaline, but not with sympathetic nerve stimulation, methoxamine or ATP, is enhanced in cirrhosis. Nitric oxide does not appear to play a modulatory role in these responses. |
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Authors:
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R T Mathie; V Ralevic; G Burnstock |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of hepatology Volume: 25 ISSN: 0168-8278 ISO Abbreviation: J. Hepatol. Publication Date: 1996 Jul |
Date Detail:
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Created Date: 1996-12-12 Completed Date: 1996-12-12 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8503886 Medline TA: J Hepatol Country: DENMARK |
Other Details:
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Languages: eng Pagination: 90-7 Citation Subset: IM |
Affiliation:
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Department of Surgery, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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pharmacology Animals Electric Stimulation Liver Cirrhosis, Experimental / physiopathology* Male Methoxamine / pharmacology NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide / physiology* Norepinephrine / pharmacology Portal Pressure / drug effects Portal System / physiopathology* Rats Rats, Wistar Sympathetic Nervous System / physiology* Vasoconstriction / drug effects |
| Chemical | |
Reg. No./Substance:
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10102-43-9/Nitric Oxide; 390-28-3/Methoxamine; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-41-2/Norepinephrine; 56-65-5/Adenosine Triphosphate |
| Comments/Corrections | |
Erratum In:
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J Hepatol 1997 May;26(5):1160-1 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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