Abstract
In recumbent man, the periodicity of adrenocorticotropin (ACTH) and plasma renin activity (PRA) is well established—a daytime downward drift with an early-morning surge. In upright man, however, the patterns differ. Although the circadian rhythm of ACTH and its effect on corticosteroids persists regardless of position, assumption of upright posture in daytime causes an increase in PRA, resulting in a biphasic pattern. The rhythms of ACTH-dependent steroids, cortisol, corticosterone, and deoxycorticosterone remain unchanged regardless of posture. In addition, aldosterone has an ACTH-dependent pattern when PRA is fixed or virtually inoperative during recumbency. However, with assumption of upright posture after overnight recumbency, the increase in PRA produces a peak in plasma aldosterone concentration and this results in a biphasic plasma aldosterone response to upright posture. During recumbency, the early-morning surges of ACTH and PRA seem to be closely related. However, with assumption of upright posture, there is clear separation between the increase in PRA and the diminishing ACTH effect that usually occurs between 8:00 A.M. and 12:00 noon, when most postural studies are undertaken.1
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Biglieri, E.G., and Lopez, J.M., 1977, Adrenocorticotropin and plasma aldosterone concentration and deoxycorticosterone in man, Ann. N.Y. Acad. Sci. 297: 361–369.
Rosier, A., Levine, L.S., Schneider, B., Novogroder, M., and New, M.I., 1977, The interrelationship of sodium balance, plasma renin activity and ACTH in congenital adrenal hyperplasia, J. Clin. Endocrinol. Metab. 45: 500–512.
Limal, J.-M., Rappaport, R., and Bayard, F., 1977, Plasma aldosterone, renin activity, and I7α-hydroxyprogesterone in salt-losing congenital adrenal hyperplasia. I. Response to ACTH in hydrocortisone treated patients and effect of 9α-fludrocortisol, J. Clin. Endocrinol. Metab. 45: 551–559.
Rösier, A., Rabinowitz, D., Theodore, R., Ramirez, L.C., and Ulick, S., 1977, The nature of the defect in a salt-wasting disorder in Jews of Iran, J. Clin. Endocrinol. Metab. 44: 279–291.
Rayyis, S.S., and Horton, R., 1971, Effect of angiotensin II on adrenal and pituitary function in man, J. Clin. Endocrinol. Metab. 32: 539–546.
Ames R.P., Borkowski, A.J., Sicinski, A.M., and Laragh, J.H., 1965, Prolonged infusions of angiotensin II and norepinephrine and blood pressure, electrolyte balance, and aldosterone and cortisol secretion in normal man and in cirrhosis with ascites, J. Clin. Invest. 44: 1171–1186.
Blair-West, J.R., Coghlan, J.P., Denton, D.A., and Scoggins, B.A., 1974, Aldosterone regulation of sodium deficiency: Role of ionic factors and angiotensin II, in: Handbook of Experimental Pharmacology, Vol. 37: Angiotensin (I.H. Page and F.M. Bumpus, eds.), pp. 337–368, Springer-Verlag, New York.
Wenting, G.J., Man in’ t Veld, A.J., Verhoeven, R.P., Derkx, F.H.M., and Schalekamp, M.A.D.H., 1977, Volume-pressure relationships during development of mineralocorticoid hypertension in man, Circ. Res. 40(Suppl. I): I–163–I–170.
Tarazi, R.C., 1976, Hemodynamic role of extracellular fluid in hypertension, Circ. Res. 38(Suppl. II): II–73–II–83.
London, G.M., Safar, M.E., Weiss, Y.A., Corvol, P.L., Lehner, J.P., Menard, J.M., Simon, A.C., and Milliez, P.L., 1977, Volume-dependent parameters in essential hypertension, Kidney Int. 11: 204–208.
Marks, L.S., Maxwell, M.H., and Kaufman, J.J., 1977, Renin, sodium, and vasodepressor response to saralasin in renovascular and essential hypertension, Ann. Intern. Med. 87: 176–182.
Wilson, H.M., Wilson, J.P., Slaton, P.E., Foster, J.H., Liddle, G.W., and Hollifield, J.W., 1977, Saralasin infusion in the recognition of renovascular hypertension, Ann. Intern. Med. 87: 36–42.
Case, D.B., Wallace, J.M., Keim, H.J., Weber, M.A., Sealey, J.E., and Laragh, J.H., 1977, Possible role of renin in hypertension as suggested by renin-sodium profiling and inhibition of converting enzyme, N. Engl. J. Med. 296: 641–646.
Mersey, J.H., Williams, G.H., Hollenberg, N.K., and Dluhy, R.G., 1977, Relationship between aldosterone and bradykinin, Circ. Res. 40(Suppl. I): I–84–I–88.
Williams, G.H., and Hollenberg, N.K., 1977, Accentuated vascular and endocrine response to SQ 20881 in hypertension, N. Engl. J. Med. 297: 184–188.
Re, R., Novelline, R., Escourrou, M.-T., Athanasoulis, C., Burton, J., and Haber, E., 1977, Inhibition of angiotensin-converting enzyme for diagnosis of renal-artery stenosis, N. Engl. J. Med. 298: 582–586.
Weber, M.A., Drayer, J.I.M., Rev, A., and Laragh, J.H., 1971, Disparate patterns of aldosterone response during diuretic treatment of hypertension, Ann. Intern. Med. 87: 558–563.
Tan, S.Y., and Mulrow, P.J., 1977, Inhibition of the renin-aldosterone response to furosemide by indomethacin, J. Clin. Endocrinol. Metab. 45: 174–176.
Speckart, P., Zia, P., Zipser, R., and Horton, R., 1977, The effect of sodium restriction and prostaglandin inhibition on the renin-angiotensin system in man, J. Clin. Endocrinol. Metab. 44: 832–837.
Halushka, P.V., Wohltmann, H., Privitera, P.J., Hurwitz, G., and Margolius, H.S., 1977, Bartter’s syndrome: Urinary prostaglandin E-like kallikrein; indomethacin effects, Ann. Intern. Med. 87: 281–286.
McGiff, J.C., 1977, Bartter’s syndrome results from an imbalance of vasoactive hormones, Ann. Intern. Med. 87: 369–372.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1979 Springer Science+Business Media New York
About this chapter
Cite this chapter
Biglieri, E.G. (1979). Renin-Angiotensin-Aldosterone. In: Ingbar, S.H. (eds) Contemporary Endocrinology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-4857-4_7
Download citation
DOI: https://doi.org/10.1007/978-1-4757-4857-4_7
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4757-4859-8
Online ISBN: 978-1-4757-4857-4
eBook Packages: Springer Book Archive