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1. 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. 2. Infusions of MgCl2 solutions into the renal artery which raised the renal plasma Mg concentration (PMg) by 0.1-2 m-mole.1.-1 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. 3. In other experiments, an increase in PMg of 1.5-2.5 m-mole.1.-1 was also found to increase renin release into lymph. 4. When the plasma Ca concentration was doubled by infusion of CaCl2 into one renal artery, an increase in PMg of 1.5-2.5 m-mole.1.-1 no longer increased renin release into plasma or lymph. 5. When the plasma NaCl concentration was raised by 8-15 m-mole.1.-1 by infusion of hypertonic saline into the renal artery, MgCl2 infusion failed to increase renin release until PMg was raised by more than 3 m-mole.1-1. 6. The results demonstrate that hypermagnesaemia stimulates renal renin release by a mechanism that is independent of the renal nerves, or of any changes in blood pressure or sodium excretion, but which is antagonized by concurrent hypercalcaemia or hypersalaemia. 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.