ArticleLiver international : official journal of the International Association for the Study of the Liver2010
A distinct nitric oxide and adenosine A1 receptor dependent hepatic artery vasodilatatory response in the CCl-cirrhotic liver.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Congestive Hepatopathy.International journal of molecular sciences · 2020Review
- Evolution in the understanding of the pathophysiological basis of portal hypertension: How changes in paradigm are leading to successful new treatments.Journal of hepatology · 2015Review
- Hepatic arterial vasodilation is independent of portal hypertension in early stages of cirrhosis.PloS one · 2015Article
- Extrahepatic complications to cirrhosis and portal hypertension: haemodynamic and homeostatic aspects.World journal of gastroenterology · 2014Review
- Purinergic signalling in the liver in health and disease.Purinergic signalling · 2014Review
- Purinergic signaling in liver disease.Digestive diseases (Basel, Switzerland) · 2014Review
- Pathological roles of purinergic signaling in the liver.Journal of hepatology · 2012Review
- Morphological and biomechanical remodelling of the hepatic artery in a swine model of portal hypertension.Hepatology international · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledIncrease of portal venous vascular resistance is counteracted by decrease of hepatic arterial vascular resistance (hepatic arterial buffer response). This process is mediated by adenosine in normal livers. In cirrhosis, hepatic arterial vascular resistance is decreased but the involvement of adenosine in this process is unknown. The aim of our study was to identify the signalling pathway responsible for the decreased hepatic arterial resistance in cirrhotic livers.
methodsCirrhosis was induced by CCl(4). Using a bivascular liver perfusion dose-response curves to adenosine of the HA were performed in the presence and the absence of pan-adenosine blocker (8-SPT), A1 blocker (caffeine) or nitric oxide synthase-blocker (l-NMMA) after preconstriction with an alpha1-agonist (methoxamine). Western blot of the HA were used to measure the density of the A1 and A2a receptors.
resultsAdenosine caused a dose dependent relaxation of the hepatic artery of both cirrhotic and control animals that were blocked in both groups by 8-SPT (P<0.02). The response to adenosine was greater in cirrhotic rats (P=0.016). Both l-NMMA (P=0.003) and caffeine reduced the response to adenosine in cirrhotic but not in control animals. Western blot analysis showed a higher density of A1 and a lower density of A2a receptor in cirrhotic animals (P<0.05).
conclusionThe adenosine-induced vasodilatation of the HA is increased in cirrhotic rats suggesting a role for adenosine-NO in the decreased hepatic arterial vascular resistance found in cirrhosis. This significantly greater response in cirrhosis by the A1 receptor follows the same pathway that is seen in hypoxic conditions in extra-hepatic tissues.
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