Role of nitric oxide in extracellular nucleotide-induced contractile status of assorted vessels including parts of the portal vasculature

Background/Aims: The resistance of portal vein and hepatic artery plays an important role in the regulation of the circulatory status in the liver, but the regulatory mechanisms for these hepatic vessels have still to be elucidated. The aim of this study was to discover the tonus regulation of the hepatic vasculature. Methods: The effects of adenosine, adenosine 5′-monophosphate, adenosine 5′-diphosphate, adenosine 5′-triphosphate and uridine triphosphate on the force generation of the portal vein, superior mesenteric artery, inferior caval vein and aorta of the rat were studied in vitro. Each vessel was removed and cut into 5-mm ring strips. The strips were fixed vertically between triangle hooks and incubated in organ baths containing Krebs-Henseleit solution. The change in vascular tension was continuously monitored by a force-displacement transducer and recovered isometrically with a polygraph. Results: Adenosine 5′-diphosphate and adenosine 5′-triphosphate induced relaxation of superior mesenteric artery and aorta precontracted with prostaglandin F2α dose-dependently. The effctects of adenosine 5′-diphosphate and adenosine 5′-triphosphate were attenuated in the presence of NG-nitro- -arginine, indicating nitric oxide dependency. In contrast, all these nucleotides dose-dependently induced contraction of the portal vein obtained from the hepatic hilus. NG-nitro- -arginine decreased the EC50 values for the metabolites. Interestingly, all the nucleotides failed to induce contraction of the inferior caval vein and the portal vein distal to the hepatic hilus. Conclusions: These results suggest that some purino-ceptor-dependent pathway regulates contraction of the portal vein close to the hepatic hilus and elicits, in contrast, the relaxation of superior mesenteric artery and aorta. Nitric oxide may participate in the tonus regulation of hepatic vasculature.