Aldosterone and Renin

  • Edward G. Biglieri
Part of the Contemporary Endocrinology book series (COE, volume 2)


To appreciate the origins of the steroids produced in the zona glomerulosa (ZG) and zona fasciculata (ZF), the reader is referred to Fig. 1. The unique steroids from the ZG are 18-hydroxycorticosterone (180H-B) and aldosterone. The contribution of ZG corticosterone (B) and deoxycorticosterone (DOC) to peripheral blood levels must be minimal because current evidence suggests that they are primarily ACTH-dependent and of ZF origin. Only in the 17α-hydroxylase deficiency type of congenital adrenal hyperplasia (CAH) does 18OH-B originate from the ZF. Angiotensin II is the principal regulator of this zone, but acute or short-term administration of ACTH stimulates 18OH-B and aldosterone.


Plasma Renin Activity Congenital Adrenal Hyperplasia Primary Aldosteronism Plasma Aldosterone Zona Glomer 
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  1. 1.
    Kuhnle, U., Chow, D., Rapaport, R., Pang, S., Levine, L. S., and New, M. I., 1981, The 21-hydroxylase activity in the glomerulosa and fasciculata of the adrenal cortex in congenital adrenal hyperplasia, J. Clin. Endocrinol. Metab. 52: 534–544.PubMedCrossRefGoogle Scholar
  2. 2.
    Biglieri, E. G., Wajchenberg, B. L., Malerbi, D. A., Okada, H., Lemme, C. E., and Kater, C. E., 1981, The zonal origins of the mineralocorticoid hormones in the 21-hydroxylation, deficiency of congenital adrenal hyperplasia, J. Clin. Endocrinol. Metab. 53: 964–969.PubMedCrossRefGoogle Scholar
  3. 3.
    Beitins, I. Z., Bayard, F., Kowarski, A., and Migeon, C. J., 1972, The effect of ACTH administration on aldosterone production in nonsalt-losing congenital adrenal hyperplasia, J. Clin. Endocrinol. Metab. 35: 595–603.PubMedCrossRefGoogle Scholar
  4. 4.
    Homer, J. M., Hintz, R. L., and Luetscher, J. A., 1979, The role of renin and angiotensin in salt-losing, 21-hydroxylase deficient congenital adrenal hyperplasia, J. Clin. Endocrinol. Metab. 48: 776–783.CrossRefGoogle Scholar
  5. 5.
    Lemal, J. M., Rapaport, R., and Bayard, F., 1976, Plasma aldosterone, renin activity, and 17a-hydroxyprogesterone in salt-losing congenital adrenal hyperplasia. I. Response to ACTH on hydrocortisone treated patients and effect of 9a-fluorocortisol, J. Clin. Endocrinol. Metab. 45: 551–559.CrossRefGoogle Scholar
  6. 6.
    Biglieri, E. G., Chang, B., Hirai, J., Brust, N., Rost, C. R., and Schambelan, M., 1979, Adrenocorticotropin inhibition of mineralocorticoid hormone production, Clin. Sci. 56: 307–311.Google Scholar
  7. 7.
    Aquilera, G., Fujita, K., and Catt, K. J., 1981, Mechanisms of inhibition of aldosterone secretion by adrenocorticotropin, Endocrinology 108: 522–526.CrossRefGoogle Scholar
  8. 8.
    Ulick, S., Eberlein, W. R., Bliffeld, A. R., Chu, M. D., and Bongioanini, A. F., 1980, Evidence for an aldosterone biosynthetic defect in congenital adrenal hyperplasia, J. Clin. Endocrinol. Metab. 51: 1346–1353.PubMedCrossRefGoogle Scholar
  9. 9.
    Sonino, N., Levine, L. S., Vecsei, P., and New, M. I., 1980, Parallelism of 1113 and 18-hydroxylation demonstrated in urinary free hormones in man, J. Clin. Endocrinol. Metab. 51: 557–560.PubMedCrossRefGoogle Scholar
  10. 10.
    Levine, L. S., Rauh, W., Gottesdiener, K., Chow, D., Gunczler, P., Rapaport, R., Pang, S., Schneider, B., and New, M.I., 1980, New studies of the 1113hydroxylase and 18-hydroxylase enzymes in the hypertensive form of congenital adrenal hyperplasia, J. Clin. Endocrinol. Metab. 50: 258–265.PubMedCrossRefGoogle Scholar
  11. 11.
    Biglieri, E. G., 1979, Mechanisms establishing the mineralocorticoid hormone patterns in the 17a-hydroxylase deficiency syndrome, J. Steroid Biochem. 11: 653–658.PubMedCrossRefGoogle Scholar
  12. 12.
    Kater, C. E., Biglieri, E. G., and Brust, N., 1981, An explanation for the sequential variation leading to the unique zona fasciculata mineralocorticoid levels in the 17a-hydroxylase deficiency, Program of Endocrinology of Hypertension Symposium, Serano, Italy, P. 34.Google Scholar
  13. 13.
    Ulick, S., 1976, Adrenocortical factors in hypertension. I. Significance of 18-hydroxy-11-deoxycorticosterone, Am. J. Cardiol. 38: 814–824.PubMedCrossRefGoogle Scholar
  14. 14.
    New, M. I., Levine, L. S., Biglieri, E. G., Pareira, J., and Ulick, S., 1977, Evidence for an unidentified steroid in a child with an apparent mineralocorticoid hypertension, J. Clin. Endocrinol. Metab. 44: 924–933.PubMedCrossRefGoogle Scholar
  15. 15.
    Ulick, S., Levine, L. S., Gunczler, P., Zanconato, G., Ramirez, L. C., Rauh, W., Roster, A., Bradow, H. L., and New, M. I., 1979, A syndrome of apparent mineralocorticoid excess associated with defects in the peripheral metabolism of cortisol, J. Clin. Endocrinol. Metab. 49: 757–764.PubMedCrossRefGoogle Scholar
  16. 16.
    Shackleton, C. H. L., Honour, J. W., Dillon, M. J., Chansler, C., and Jones, R. W. A., 1980, Hypertension in a four year old child: Gas chromatographic and mass spectrometric evidence for deficient hepatic metabolism of steroids, J. Clin. Endocrinol. Metab. 50: 786–792.PubMedCrossRefGoogle Scholar
  17. 17.
    Vingerhoeds, A. C. M., Thijssen, J. H. H., and Schwartz, F., 1976, Spontaneous, hypercortisolism without Cushing’s syndrome, J. Clin. Endocrinol. Metab. 43: 1128–1133.PubMedCrossRefGoogle Scholar
  18. 18.
    Chrousos, C. P., Vingerhoeds, A., Brandon, D., de Regt, J., Pugeat, M., Eli, C., Loriaux, D. L., and Lipsett, M. B., 1981, Primary cortisol resistance: A glucocorticoid receptor-mediated disease, 33rd Annual Meeting of the Endocrine Society, p. 276.Google Scholar
  19. 19.
    Biglieri, E. G., and Schambelan, M., 1979, Significance of elevated levels of plasma hydroxycorticosterone in patients with primary aldosteronism, J. Clin. Endocrinol. Metab. 49: 87–91.PubMedCrossRefGoogle Scholar
  20. 20.
    Biglieri, E. G., and Baxter, J. D., 1981, The endocrinology of hypertension, in: Endocrinology and Metabolism (B. Felig, J. D. Baxter, A. Broadus, and L. Frohman, eds. ), p. 551.Google Scholar
  21. 21.
    Vetter, H., Siebenschein, R., Stude, A., Witassek, F., Furrer, J., Glanzer, L., Siegenthaler, W., and Vetter, W., 1979, Primary aldosteronism: Inability to differentiate unilateral from bilateral adrenal type lesions by various routine clinical and laboratory data and by peripheral plasma aldosterone, Acta Endocrinol. (Copenhagen) 89: 710–725.Google Scholar
  22. 22.
    Weinberger, N. H., Grim, C. E., Hollifield, J. M., Kern, D. C., Ganguly, A., Kramer, N. J., Yume, N. H., Wellman, H., and Donohue, J. P., 1979, Primary aldosteronism: Diagnosis, localization and treatment, Ann. Intern. Med. 90: 386–395.PubMedGoogle Scholar
  23. 23.
    Vaughan, N. J. A., Slater, J. D. H., Lightman, S., Jowett, T. P., Wiggins, R. C., Ma, J. T. C., and Payne, N. N., 1981, The diagnosis of primary hyperaldosteronism, Lancet 1: 120–125.PubMedCrossRefGoogle Scholar
  24. 24.
    White, E. A., Schambelan, M., Sigala, J. F., Glynn, R. D., and Biglieri, E. G., 1980, Use of computed tomography in diagnosing the cause of primary aldosteronism, N. Engl. J. Med. 303: 1503–1507.PubMedCrossRefGoogle Scholar
  25. 25.
    Wisgerhoff, M., Carpenter, P. C., and Brown, R. D., 1978, Increased adrenal sensitivity to angiotensin II in idiopathic hyperaidosteronism, J. Clin. Endocrinol. Metab. 47: 938–943.CrossRefGoogle Scholar
  26. 26.
    Kern, D. C., Weinberger, M. H., Higgins, J. R., Kramer, N. J., Gomez-Sanchez, C., and Holland, O. B., 1978, Plasma aldosterone response to ACTH in primary aldosteronism and patients with low renin hypertension, J. Clin. Endocrinol. Metab. 46: 552–560.CrossRefGoogle Scholar
  27. 27.
    Carey, R. M., Thorner, M. O., and Ortt, E. M., 1980, Dopaminergic inhibition of metoclopramide-induced aldosterone secretion in man, J. Clin. Invest. 66: 10–18.PubMedCrossRefGoogle Scholar
  28. 28.
    Noth, R. H., McCallum, R. W., Contino, C., and Havelick, J., 1980, Tonic dopaminergic suppression of plasma aldosterone, J. Clin. Endocrinol. Metab. 51: 64–69.PubMedCrossRefGoogle Scholar
  29. 29.
    Kuchel, O., Buu, N. T., Vescei, P., Bourque, M., Harnet, P., and Genest, J., 1980, Are plasma aldosterone surges in primary aldosteronism due to a loss of an inhibiting dopaminergic control? J. Clin. Endocrinol. Metab. 51: 337–343.PubMedCrossRefGoogle Scholar
  30. 30.
    Vinson, G. P., Whitehouse, B. J., Dell, A., Etienne, T., and Morris, H. R., 1980, Characterization of an adrenal zona glomerulosa-stimulating component of posterior pituitary extracts as a-MSH, Nature (London) 284: 464–467.CrossRefGoogle Scholar
  31. 31.
    Matsuoka, H., Mulrow, P.J., and Li, C. H., 1980, Beta-lipotropin: A new aldosterone-stimulating factor, Science 209: 307–308.PubMedCrossRefGoogle Scholar
  32. 32.
    Lis, M., Hamet, P., Gutkowska, J., Maurice, G., Seidah, N. G., Larivere, N., Chretien, M., and Genest, J. 1981, Pro-opiomelanocortin in aldosterone release by human adrenal adenoma in vitro, J. Clin. Endocrinol. Metab. 52: 1053–1056.PubMedCrossRefGoogle Scholar
  33. 33.
    Sen, S., Valenzuela, R., Smeby, R., Bravo, E., and Bumpus, F. M., 1981, Localization, purification and biological activity of a new aldosterone stimulating factor, Hypertension 3 (Suppl. I): I81–I89.PubMedGoogle Scholar
  34. 34.
    Brown, J. J., Lever, A. F., Robertson, J. I. S., Beeveb, D. G., Cumming, A. M., Davies, D. L., Fraser, R., Mason, P., Morton, J. S., Tree, M., 1979, Are idiopathic hyperaldosteronism and low-renin hypertension variants of essential hypertension?, Ann. Clin. Biochem. 16: 380–388.PubMedGoogle Scholar
  35. 35.
    Gill, J. R., Jr., and Bartter, F. C., 1981, Overproduction of sodium retaining steroids by the zona glomerulosa is adrenocorticotropin-dependent and mediates hypertension in dexamethasone-suppressible aldosteronism, J. Clin. Endocrinol. Metab. 53: 335–337.CrossRefGoogle Scholar
  36. 36.
    Rauh, W., Levine, L. S., Gottesdiener, K., and New, M. I., 1978, Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension, Klin. Wochenschr. 56 (Suppl. I): 161–167.PubMedCrossRefGoogle Scholar
  37. 37.
    Lau, N. C., Matulich, D. T., Stockigt, J. R., Biglieri, E. G., New, M. I., Wenter, J. S. D., McKenzie, J. K., and Baxter, J. D., 1980, Radioreceptor assay of plasma mineralocorticoid activity: Role of aldosterone, cortisol, deoxycorticosterone in various mineralocorticoid excess states, Circ. Res. 46 (Suppl. I): I94–I100.Google Scholar
  38. 38.
    Oberfield, S. E., Levine, L. S., Stoner, E., Chow, D., Rauh, W., Greig, F., Lee, S. M., Lightner, E., Witte, M., New, M. I., 1981, Adrenal glomerulosa function in patients with dexamethasone-suppressible hyperaldosteronism, J. Clin. Endocrinol. Metab. 53: 158–164.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Publishing Corporation 1985

Authors and Affiliations

  • Edward G. Biglieri
    • 1
    • 2
  1. 1.Endocrinology Service of the Medical Services, and Clinical Study CenterSan Francisco General Hospital Medical CenterSan FranciscoUSA
  2. 2.Department of MedicineUniversity of California School of MedicineSan FranciscoUSA

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