Effects of Changes in Serum Calcium and Parathyroid Hormone on Plasma Renin in Intact Mongrel Dogs

Abstract

Studies were undertaken to extend previous experiments of the interaction between calcium and parathyroid hormone 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 ± 0.85 ng/ml/h in 17 normotensive dogs compared to 1.52 ± 0.29 ng/ml/h in 14 normocalcemic normotensive dogs (p < 0.05). In 5 renovascular dogs, calcium-channel antagonism with nifedipine resulted in a higher PRA of 31.8 ± 0.5 compared to 11.9 ± 1.1 ng/ml/h in 23 control renovascular dogs not receiving nifedipine (p < 0.001). The reactive hyperreninemia following angiotensin blockade was greater in 22 hypocalcemic (10.94 ± 2.03 ng/ ml/h) normotensive dogs compared to 14 normocalcemic normotensive dogs (1.32 ± 0.34 ng/ml/h, p < 0.001). Similar results were obtained with angiotensin blockade in nifedipine-treated animals compared to angiotensin blockade in nonnifedipine-treated normotensive dogs. Results with angiotensin blockade on PRA levels in renovascular dogs were found similar to those described with angiotensin blockade in normotensive dogs. We conclude from these studies that calcium reduction, independent of a rise in parathyroid hormone, or calcium-channel blockade was associated with an elevation of PRA in normotensive 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 (consisting either of serum calcium reduction or calcium-channel blockade). Finally, hypocalcemia and calcium-channel blockade resulted in greater reactive hyperreninemia after angiotensin blockade in both groups of dogs.