The effects of changes in serum calcium and parathormone on plasma renin activity in intact mongrel dogs.

Abstract

Studies were undertaken to extend previous observations of the interaction between calcium and parathormone on renin synthesis by the kidney. Intact normovolemic mongrel dogs between 15 and 25 kg were used for all studies. Plasma renin activity (PRA) was measured by radioimmunoassay. Hypocalcemia produced by thyroparathyroidectomy or chelation with EDTA resulted in an elevated PRA of 3.76 +/- .86 ng/ml/hr in 17 dogs compared to 1.5 +/- .29 ng/ml/hr in 14 controls (p less than .05). In 5 renovascular dogs calcium-channel blockade with nifedipine resulted in a higher PRA of 31.8 +/- 0.5 compared to 11.9 +/- 1.1 ng/ml/hr in 23 renovascular controls, p less than .001. The reactive hyperreninemia following angiotensin blockade was greater in 22 hypocalcemic (10.94 +/- 2.03 ng/ml/hr) dogs compared to 14 controls (1.32 +/- .34 ng/ml/hr), p less than .001. Results with calcium antagonism on PRA levels in renovascular dogs were found similar to those described with angiotensin blockade. We conclude from these studies that calcium-channel blockade or calcium reduction independent of a rise in parathormone was associated with an elevation of PRA in normal and renovascular hypertensive dogs. The rise in PRA could occur without changes in blood pressure or volume, consistent with an interruption of the short feedback loop control of renin synthesis by calcium antagonism. Finally, hypocalcemia and calcium-channel blockade resulted in reactive hyperreninemia greater than or equal to that seen after angiotensin blockade in both groups of dogs, again suggesting interference with the short feedback loop control of renin synthesis.