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. 1994 Jun;93(6):2691-700.
doi: 10.1172/JCI117283.

Altered adenylyl cyclase activities and G-protein abnormalities in portal hypertensive rabbits

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Altered adenylyl cyclase activities and G-protein abnormalities in portal hypertensive rabbits

P A Cahill et al. J Clin Invest. 1994 Jun.

Abstract

Portal hypertension (PHT) is characterized by splanchnic hyperemia due to a reduction in mesenteric vascular resistance. We hypothesized that alterations in the activity of a guanine-nucleotide regulatory protein (G-protein) might be partially responsible for the marked circulatory disturbances observed in PHT. We, therefore, determined alterations in adenylyl cyclase/cAMP system in prehepatic portal hypertensive rabbits and correlated these changes to the activity of a G-protein. Basal and G-protein-stimulated adenylyl cyclase activities were lower in the PHT superior mesenteric artery (22-26%) and thoracic aorta (31-46%) membranes, but higher (178-321%) in portal vein. The functional activity of Gi alpha proteins (pertussis toxin-catalyzed ADP-dependent ribosylation) increased in the PHT superior mesenteric artery and thoracic aorta, but decreased in portal vein. Immunodetection revealed an increase in the Gi alpha protein subunits (Gi alpha 1/Gi alpha 2 and Gi alpha 3/Go alpha) in PHT thoracic aorta, without any change in Gs alpha proteins; and a decrease in the amount of Gi alpha proteins in PHT portal vein. There was no change in the amount of Gs alpha/Gi alpha in the PHT superior mesenteric artery. We conclude the hemodynamic alterations of PHT are associated with intrinsic alterations in G-protein-enzyme effector systems. These alterations are vessels specific and suggest a possible unique global derangement underlying the vasculopathy of PHT.

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References

    1. Am J Physiol. 1985 Feb;248(2 Pt 1):G192-5 - PubMed
    1. Am J Physiol. 1983 Jan;244(1):G52-7 - PubMed
    1. Br J Clin Pharmacol. 1986 Feb;21(2):191-6 - PubMed
    1. Lancet. 1986 Jun 21;1(8495):1409-11 - PubMed
    1. FEBS Lett. 1986 Jun 23;202(1):63-8 - PubMed

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