Prostaglandin responses in isolated perfused rat liver: Ca2+ and K+ fluxes, hemodynamic and metabolic effects.
Addition of prostaglandin F2 alpha and prostaglandin E2 to isolated perfused rat liver led to a dose-dependent, transient net Ca2+ release, which was completed within 3 min. Withdrawal of the prostaglandins resulted in a Ca2+ re-uptake over a period of about 10 min. Simultaneously, these prostaglandins induced an increase of portal pressure, stimulated hepatic glucose output and 14CO2 production from [1-14C]glutamate and led to K+ movements across the hepatocyte plasma membrane similar to those observed with other Ca2+-mobilizing agents. With prostaglandin F2 alpha there was a close correlation between the net Ca2+ release and the maximal rate of initial net K+ uptake by the liver (linear regression coefficient r = 0.902; n = 20). Prostaglandin F2 alpha was more effective than prostaglandin E2 or D2. Because prostaglandins are known to be produced by hepatic non-parenchymal cells during stimulation by phagocytosis or by addition of extracellular ATP or UTP, these data suggest an interaction between non-parenchymal and parenchymal liver cells and point to a modulating role of prostaglandins in hepatic metabolism and microcirculation, which is mediated by Ca2+-mobilizing mechanisms.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015237:Dinoprost; D015232:Dinoprostone; D066298:In Vitro Techniques; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008102:Liver Circulation / Q000187:drug effects; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D011460:Prostaglandins F / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D015237:Dinoprost; D015232:Dinoprostone; D011188:Potassium; D002118:Calcium