INCREASED NITRIC-OXIDE SYNTHASE - EXPRESSION IN ARTERIAL VESSELS OF CIRRHOTIC RATS WITH ASCITES

Citation
M. Moralesruiz et al., INCREASED NITRIC-OXIDE SYNTHASE - EXPRESSION IN ARTERIAL VESSELS OF CIRRHOTIC RATS WITH ASCITES, Hepatology, 24(6), 1996, pp. 1481-1486
Citations number
44
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
24
Issue
6
Year of publication
1996
Pages
1481 - 1486
Database
ISI
SICI code
0270-9139(1996)24:6<1481:INS-EI>2.0.ZU;2-5
Abstract
Arterial vasodilatation is thought to play a major role in the pathoge nesis of systemic hemodynamics and renal disturbances occurring in cir rhotic patients. Recent investigations suggest that an increased vascu lar nitric oxide (NO) production could be implicated in this abnormali ty. The current study assessed whether increased expression of inducib le and/or endothelial nitric oxide synthase (iNOS and eNOS, respective ly) occurs in arterial vessels of cirrhotic rats. The investigation wa s performed in thoracic and abdominal aortas and mesenteric arteries o f 10 control rats and 16 cirrhotic rats with ascites. iNOS and eNOS me ssenger RNA (mRNA) expression were evaluated by polymerase chain react ion and ribonuclease protection assay, respectively. Endothelial NOS p rotein expression was assessed by Western blot. No iNOS mRNA was detec ted in arterial vessels of control rats. In contrast iNOS mRNA was con sistently detected in all arteries of cirrhotic rats with ascites, the weakest signal being observed in the thoracic aorta and the strongest in the mesenteric artery. Enhanced eNOS mRNA abundance was found in t he aorta of cirrhotic animals as compared with controls. Higher eNOS p rotein expression was noted in the thoracic aorta of cirrhotic rats. T hese results indicate the existence of increased eNOS and iNOS express ion in arterial vessels of cirrhotic rats, suggesting that transcripti onal activation of vascular NOSs and the associated nitric oxide hyper production may be of major importance in the pathogenesis of arterial vasodilation in cirrhosis.