Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

Heinemann, A; Wachter, CH; Holzer, P; Fickert, P; Stauber, RE.
Nitric oxide-dependent and -independent vascular hyporeactivity in mesenteric arteries of portal hypertensive rats.
Br J Pharmacol. 1997; 121(5):1031-1037 Doi: 10.1038/sj.bjp.0701220 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Führende Autor*innen der Med Uni Graz
Heinemann Akos
Co-Autor*innen der Med Uni Graz
Fickert Peter
Holzer Peter
Stauber Rudolf
Altmetrics:

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Abstract:
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.
Find related publications in this database (using NLM MeSH Indexing)
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 Muscle, Smooth, Vascular - physiology
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - physiology
Nitric Oxide Synthase - antagonists and inhibitors
Rats -
Rats, Sprague-Dawley -
Vasoconstrictor Agents - pharmacology
Vasodilator Agents - pharmacology

Find related publications in this database (Keywords)
Portal Hypertension
Mesenteric Arterial Bed
Nitric Oxide
Noradrenaline
Methoxamine
Arginine Vasopressin
Endothelin-1
5-Hydroxytryptamine
Indomethacin
N-G-Nitro-L-Arginine Methyl Ester (L-Name)
© Med Uni Graz Impressum