To determine whether glucagon affects the plasma concentration of urid
ine, we administered 100 mL physiological saline containing 1 mg gluca
gon or 100 mt physiological saline alone intravenously over 1 hour to
healthy subjects. Glucagon decreased the plasma concentration of uridi
ne from 5.72 +/- 1.05 to 4.80 +/- 0.60 mu mol/L but increased the conc
entrations of cyclic adenosine monophosphate (cAMP) in plasma and pyru
vic acid and lactic acid in blood 59-, 1.4-, and 1.3-fold, respectivel
y. Although glucagon increased urinary excretion of uric acid, it did
not affect the plasma concentration of purine bases (hypoxanthine, xan
thine, and uric acid) or urinary excretion of oxypurines and uridine,
indicating that glucagon does not affect purine degradation and sugges
ting that glucagon does not affect adenosine triphosphate (ATP) consum
ption-induced pyrimidine degradation. In contrast, physiological salin
e did not affect any of the measured variables. These results suggest
that glucagon enhanced Na+-dependent uridine uptake from the blood int
o the cells, since glucagon stimulates Na+-dependent uridine uptake in
to cells in vitro. Copyright (C) 1998 by W.B. Saunders Company.