The Effects of Changes in Serum Calcium and Parathormone on Plasma Renin Activity in Intact Mongrel Dogs

  • Edward T. ZawadaJr.
  • Michael Johnson
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 178)


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< .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< .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< .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.


Renal Artery Serum Calcium Plasma Renin Activity Renovascular Hypertension Significant Fall 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    G. S. Brinton, W. Jubiz, and L. D. Lagerquist, Hypertension in primary hyperparathyroidism: The role of the renin-angiotensin system, J. Clin. Endocrinol. Metab. 41: 1025 (1975).PubMedCrossRefGoogle Scholar
  2. 2.
    E. T. Zawada, Jr., A. S. Brickman, M. H. Maxwell, and M. A. Tuck, Hypertension associated with hyperparathyroidism is not responsive to angiotensin blockade, J. Clin. Endocrinol. Metab. 50: 912 (1980).PubMedCrossRefGoogle Scholar
  3. 3.
    D. S. Chen, and A. M. Poisner, Direct stimulation of renin release by calcium, Proc. Soc. Exp. Biol. Med. 152: 565 (1976).PubMedGoogle Scholar
  4. 4.
    J. S. Fray, Stimulation of renin release in the perfused kidney by low calcium and high magnesium, Am. J. Physiol. 237: F377 (1977).Google Scholar
  5. 5.
    E. T. Zawada, Jr., E. P. Bennett, M. Johnson, and D. Bennett, Effects of changes in serum calcium on blood pressure in conscious dogs, Nephron 33: 260 (1983).Google Scholar
  6. 6.
    E. T. Zawada, Jr., M. Johnson, Does calcium mediate high renin renal hypertension?, Clin. Res. 30: 467A (1982).Google Scholar
  7. 7.
    M. H. Maxwell, P. Varady, E. T. Zawada, Jr., J. F. Burkhalter, U. Waks, L. S. Marks, Maximal discrimination of renovascular from essential hypertension by the saralasin test, Clin. Sci. Mol. Med. 55: 2975 (1978).Google Scholar
  8. 8.
    D. B. Case, and J. H. Laragh, Reactive hyperreninemia in renovascular hypertension after blockade with saralasin or converting enzyme inhibitor, Ann. Intern. Med. 91: 153 (1979).PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1984

Authors and Affiliations

  • Edward T. ZawadaJr.
    • 1
  • Michael Johnson
    • 1
  1. 1.McGuire VA Medical CenterMedical College of VirginiaRichmondUSA

Personalised recommendations