PHOSPHATE AND CALCIUM-UPTAKE BY MITOCHONDRIA AND BY PERFUSED-RAT-LIVER INDUCED BY THE SYNERGISTIC ACTION OF GLUCAGON AND VASOPRESSIN

Co-administration of glucagon and vasopressin to rat liver perfused with buffer containing 1.3 mM-Ca2+ induces a 4-fold increase in P(i) in the subsequently isolated mitochondria (approx. 9 to approx. 40 nmol/mg of mitochondrial protein). This increase is not attributable to PP(i) hydrolysis, and is not observed if the perfusate Ca2+ is lowered from 1.3 mM to 50 μM. The increase in mitochondrial P(i) closely parallels that of mitochondrial Ca2+; when the increase in P(i) and Ca2+ accumulation is maximal, the molar ratio is close to that in Ca3(PO4)2. Measurement of changes in the perfusate P(i) revealed that, whereas administration of glucagon or vasopressin alone brought about a rapid decline in perfusate P(i), the largest decrease (reflecting net retention of P(i) by the liver) was observed when the hormone was co-administered in the presence of 1.3 mM-Ca2+. The synergistic action of glucagon plus vasopressin was nullified by lowering the perfusate Ca2+ to 50 μM. The data provide evidence that, whereas glucagon may be able to alter P(i) fluxes directly in intact liver, any alterations induced by vasopressin are indirect and result only from its action of mobilizing Ca2+.