| Nitric oxide-dependent and -independent vascular hyporeactivity in mesenteric arteries of portal hypertensive rats. | |
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MedLine Citation:
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PMID: 9222564 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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1. Increased production of nitric oxide (NO) has been suggested to underlie both the vascular hyporeactivity to vasoconstrictors and the splanchnic vasodilatation seen in portal hypertension. This study assessed the role of NO in the vasoconstrictor hyporeactivity of portal vein-ligated (PVL) rats in isolated and in situ perfused mesenteric arterial beds. 2. Isolated perfused mesenteric arteries of PVL rats were significantly less reactive to noradrenaline (NA), methoxamine (METH), arginine vasopressin (AVP) and endothelin-1 (ET-1) than those from sham-operated (Sham) rats. 3. Blockade of NO synthesis with NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) in isolated perfused mesenteric arteries from PVL rats restored the reactivity to bolus injections of AVP and ET-1, but had little effect on the hyporeactivity to NA or METH. Cyclo-oxygenase inhibition with indomethacin (5 microM) likewise did not restore reactivity to METH of isolated perfused mesenteric arteries of PVL rats. 4. The hyporeactivity to METH seen in isolated perfused mesenteric arteries from PVL rats was reduced by low concentrations of AVP (20 nM) or ET-1 (1 nM) which per se caused only a slight increase in perfusion pressure. When L-NAME (100 microM) was combined with AVP (20 nM) or ET-1 (1 nM), respectively, reactivity to METH of isolated perfused mesenteric arteries of PVL rats was restored to the level seen in Sham rats. These effects of AVP and ET-1 were not mimicked by precontracting the vessels with 5-hydroxytryptamine (5 microM). 5. The differential effects of L-NAME and AVP on the hyporesponsiveness to methoxamine and AVP were corroborated by experiments performed with the in situ perfused mesenteric vascular bed preparation. 6. These data indicate that both NO-dependent and NO-dependent mechanisms are involved in the vasoconstrictor hyporesponsiveness of mesenteric arteries from portal hypertensive rats. The hyporeactivity to AVP and ET-1 is mediated by NO whereas the reduced responsiveness to adrenoceptor agonists appears to be predominantly NO-independent AVP and ET-1, in addition, seem to inhibit the NO-independent mechanism of vascular hyporeactivity, since the hyporesponsiveness to METH was reduced in the presence of AVP or ET-1 and abolished by the combination of these peptides with L-NAME. |
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Authors:
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A Heinemann; C H Wachter; P Holzer; P Fickert; R E Stauber |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: British journal of pharmacology Volume: 121 ISSN: 0007-1188 ISO Abbreviation: Br. J. Pharmacol. Publication Date: 1997 Jul |
Date Detail:
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Created Date: 1997-09-15 Completed Date: 1997-09-15 Revised Date: 2008-11-20 |
Medline Journal Info:
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Nlm Unique ID: 7502536 Medline TA: Br J Pharmacol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 1031-7 Citation Subset: IM |
Affiliation:
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Department of Experimental and Clinical Pharmacology, Universitätsplatz 4, Graz, Austria. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arginine Vasopressin / pharmacology Blood Pressure / drug effects Endothelin-1 / pharmacology Enzyme Inhibitors / pharmacology Hemodynamics / physiology Hypertension, Portal / physiopathology* Male Mesenteric Arteries / physiopathology* Methoxamine / pharmacology Muscle, Smooth, Vascular / drug effects, physiology* NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide / physiology* Nitric Oxide Synthase / antagonists & inhibitors Rats Rats, Sprague-Dawley Vasoconstrictor Agents / pharmacology Vasodilator Agents / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Endothelin-1; 0/Enzyme Inhibitors; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 113-79-1/Arginine Vasopressin; 390-28-3/Methoxamine; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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