The effect of increasing the plasma magnesium concentration on renin release from the dog's kidney: interactions with calcium and sodium.

Abstract

A denervated auto-transplanted dog''s kidney preparation was developed to study renin release into renal plasma and lymph. The function of the transplant was compared with that of its partner. In the basal state it had a similar rate of plasma and urine flow, Na, Ca, Mg and Cl excretion but a lower rate of glomerular filtration and K excretion and a lower urinary osmolality. In the basal state the transplant did not release renin into plasma, but invariably released it into lymph. Infusions of MgCl2 solutions into the renal artery which raised the renal plasma Mg concentration (PMg) by 0.1-2 mM provoked a concentration-related increase in renin release into plasma. This was due to a rise in the veno-arterial renin difference and in the renal plasma flow rate. Blood pressure and Na excretion were unaltered. In other experiments, an increase in PMg of 1.5-2.5 mM was also found to increase renin release into lymph. When the plasma Ca concentration was doubled by infusion of CaCl2 into the renal artery, an increase in PMg of 1.5-2.5 mM no longer increased renin release into plasma or lymph. When the plasma NaCl concentration was raised by 8-15 mM by infusion of hypertonic saline into the renal artery, MgCl2 infusion failed to increase renin release until PMg was raised by more than 3 mM. Hypermagnesemia stimulates renal renin release by a mechanism that is independent of the renal nerves, or of any changes in blood pressure or Na excretion, but which is antagonized by concurrent hypercalcemia or hypersalemia. The possibility is discussed that Mg is reabsorbed from the tubular into the interstitial fluid where it antagonizes the action(s) of Ca on renin release from the juxtaglomerular cells.