Abstract
In marked contradistinction to the normal dog, to the dog with renal hypoperfusion, or to the chronic caval dog with ascites, the intravenous infusion of glucagon at 5 μg/min to dogs with experimental portal cirrhosis and ascites does not increase glomerular filtration rate or renal blood flow. In eight experimental dogs who did not respond to glucagon, a marked natriuresis was observed in response to furosemide and a marked renal vasodilator response was seen following the intraarterial infusion of acetylcholine. Because plasma immunoreactive glucagon levels are increased fivefold in cirrhotic dogs, it is suggested that continuous high levels of this peptide render the animals insensitive to the effects of an exogenous infusion.