Sodium depletion, renal denervation, beta adrenergic blockage and renin secretion and synthesis.

The role of the macula densa in the control of renin synthesis during sodium depletion was studied in Balb/c mice which had their left kidney made hydronephrotic 6 weeks earlier. The role of the nervous system was studied by giving the mice propranolol or by denervation of the left kidney. There was no net secretion of renin from the left hydronephrotic kidney on control or low sodium diet. All plasma renin came from the right kidney. Sodium depletion caused similar rises in renin content of the normal and hydronephrotic kidney. These rises were accompanied by increases in mRNA for renin in both kidneys. Denervation of the left hydronephrotic kidney caused a fall in renal renin content. However, sodium depletion caused a significant rise in both renin mRNA and renal renin in the control and denervated hydronephrotic kidney. Propranolol decreased the renin content of normal and hydronephrotic kidneys. Sodium depletion caused a rise in mRNA and renal renin in both kidneys although the absolute final amount was less than in the control animals. Sodium depletion stimulates renin synthesis in a normal kidney and a kidney without a macula densa. This response is not affected by the nervous supply to the kidney. In the hydronephrotic mouse subjected to sodium depletion the synthesis and secretion of renin appear to be disassociated.