Urinary sodium and calcium in various dog models and relationship to endogenous plasma glucagon.

Clearance studies were performed in 23 dogs undergoing extracellular volume (ECV) expansion by saline in order to evaluate relationship between endogenous glucagon and renal excretion of sodium and calcium. In control animals plasma glucagon (pG1) rose following 120 minutes of ECV expansion and was further increased by additional infusion of arginine. In pancreatectomised dogs ECV expansion failed to increase pG1. Both fractional and absolute urinary excretion of sodium in pancreatectomised dogs were markedly lower compared to control dogs. The difference in renal sodium excretion between control and pancreatectomised animals cannot be explained by the sum of nonhormonal factors influencing sodium excretion. In thyro-parathyroidectomised dogs renal sodium excretion was lower than in control dogs, but significantly higher than in pancreatectomised dogs. The arginine-induced increase of glucagon was associated with an increase of renal sodium and calcium excretion in each group under study without any change in glomerular filtration rate. In control dogs all parameters of renal sodium and calcium excretion investigated in this study were linearly correlated. Thyro-parathyroidectomy did not influence the relationship between renal sodium and calcium excretion. Hyperglucagonaemia therefore might be one factor contributing to the hypercalciuria associated with renal stone formation. In pancreatectomised dogs undergoing ECV expansion there was no significant correlation between renal sodium and calcium excretion. Pancreatic hormones might be involved in the coupling of renal sodium and calcium excretion.