Effect of extracellular UTP in rat liver: A new Ca++ linked receptor ?
Transcript of Effect of extracellular UTP in rat liver: A new Ca++ linked receptor ?
61 EFFECT OF EXTRACELLULAR UTP IN RAT LIVER: A NEW CA ++ LINKED RECEPTOR ?
D. H~ussln~er t Th. Stehle r W. Gerok Medlzlnlsche Universltatsklinik Frelburg,
W. Germany
In isolated perfused rat liver the effects of extracellular urldine triphosphate (UTP)
in mlcromolar concentratlons were studied. Extracellular UTP is very vasoactlve: concen-
tratlons as low as 1 uM were sufflcient to increase the portal pressure by about 100%.
Further, UTP (20 uM) induced a characteristic sequence of K + movements across the liver
plasma membrane, led to an inhlbltlon of oxygen consumptlon and stimulated glycogenolysls.
It further led to a prolonged Ca ++ mobil~satlon from the liver, whereas the cycllc AMP
levels were largely unaffected. Withdrawal of extracellular UTP was followed by a
transient, but pronounced stlmulatlon of glucose and K + output, the latter being followed
by a slow K + reuptake. These effects were qualitatively and quantltatlvely different from
those observed wlth extracellular ATP, which acts on the known purlnerglc P2-receptors in
llver. The UTP effects were also observed when the purlnerglc P2-receptor was maximally
stimulated by ATP. The data suggest the exlstence of a yet unknown "pyrlmldinerglc"
receptor in the liver, which, linked to a Ca++-mobillzlng mechanism, influences llver
hemodynamlcs and metabollsm (H~{ussinger eta]. (1987) Eur. J. ~1ochem. in press).
62 IONG-TE~M IMMUNE ~ ~ HBV INFECTION.
R.A. Heijtink (i), G.A. de Wilde (i), S.W. Schalm (2), F.J.W. ten Kate (3). Departments of Virology (I), Internal M~Kiicine II (2), Era~nus University Rotterdam, Dr. Molewaterplein 50, 3015 GD Rotterdam, The Netherlands.
After hepatitis B infection the long-temm persistence of HBV an~es especially against recently detected preS2 antigen is poorly documented. Therefore, we investigated sera from 39 patients 1-8 ~ after recovery frcm acute hepatitis B. PreS2 anti]xxi[es w~re detected by Western blot using virus antigen produced by CHO cells transfected with preS and S regicns of t_he HBV gencme. Anti-HBc, anti-HBs and anti-HBe were detected by ccmrercial RIAs (Abbott). Results. All samples were anti-HBc positive at dilution i:i0, but only two had a titre >i:i000. The titre of anti-HBc correlated well with the presence of anti-HBe (p=0.03). Anti-HBs %~s detected in 92% (36/39) of the sera usually with titres less than i00 IU/L. Anti-preS2 (Gp34) %~s detected in 62% but importantly in 5 out of i0 sera with anti-HBs <i0 IU/L. Strong anti-preS2 responses were only seen in sera with anti-HBs >50 IU/L. In two sera with anti-HBs >i000 IU/L however, a weak anti-S (p22, gp 26) respcnse was found together with a strong anti-preS2 ~ e . Conclusions. Ant/]xxiies against envelope and core proteins persists surprisingly long after acute hepatitis B. In contrast to the similar immune response of anti-HBc and anti-HBe, antipreS2 ~ e reactivity may be regulated independently frcm anti-S. Table. Frequency distribution of HBV antibody response with time after recovery. Time after Anti-HBs Anti- Anti- Anti-HBc recovery n >i0 IU/L >I00 IU/L preS2 HBe (>i:I00) 12 yr 13 10 3 9 7 6 3-4 yr 13 9 2 6 4 7 5-8 yr 13 ii 6 10 8 7
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