Skip to main content
Log in

Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension

Einfluß von chronischer ACTH-Behandlung auf Mineralocorticoide, Salzhaushalt und Blutdruck bei jugendlichen Hypertonikern

  • Published:
Klinische Wochenschrift Aims and scope Submit manuscript

Zusammenfassung

Der Einfluß einer 5tägigen ACTH-Behandlung (40 U/24 h) auf Plasma-Aldosteron (Aldo), Deoxycorticosteron (DOC), Plasma-Reninaktivität (PRA), auf die Ausscheidung des Aldosteron-pH-1 Conjugates (pH-1-aldo) und auf Tetrahydro-DOC (TH-DOC) wurde untersucht in Gruppe I: acht normotensiven Kindern; Gruppe II: acht Patienten mit Bluthochdruck unklarer Genese; Gruppe III: vier hypertensiven Kindern mit Dexamethason-supprimierbarem Hyperaldosteronismus (DSH). Änderungen des Blutdruckes und der Natriumbilanz wurden in allen Gruppen untersucht. Ohne Behandlung bestand kein Unterschied zwischen den Gruppen I und II. Die Kinder der Gruppe III hingegen zeigten erniedrigte PRA und eine 1,5–2fache Erhöhung des Aldo und DOC. Plasma-DOC und TH-DOC im Urin stiegen kontinuierlich auf das 10–50fache in allen Gruppen während des ACTH-Tests an. Aldo war am 1. Tag des Tests vorübergehend um das 2–4fache erhöht und fiel anschließend unter die Ausgangswerte in den Gruppen I und II. Die Kinder mit DSH (Gruppe III) zeigten eine ungewöhnliche, anhaltende Stimulation des Aldo unter ACTH-Behandlung. PRA war in den Gruppen I und II signifikant erniedrigt. Natriumretention und Anstieg des Blutdruckes wurden in allen Gruppen während des ACTH-Tests festgestellt. Die höchsten Blutdruckanstiege (von 125/72 auf 139/90) wurden in Gruppe III beobachtet. Das Ansprechen des Blutdruckes auf ACTH war zum Teil abhängig vom Natrium. Obgleich Aldo, DOC und Natriumretention wahrscheinlich zu dem ACTH-induzierten Blutdruckanstieg beitragen, müssen noch weitere Faktoren zu dessen Entstehung beitragen.

Summary

The effect of a 5 day ACTH test (40 U/24 h) on plasma aldosterone (aldo), deoxycorticosterone (DOC), plasma renin activity (PRA) and urinary excretion of aldosterone-pH1-conjugate (pH-1-aldo) and tetrahydro-DOC (TH-DOC) was investigated in 8 normotensive children (group I), 8 patients with hypertension of unknown origin (group II), and 4 hypertensive children with dexamethasone suppressible hyperaldosteronism (DSH) (group III). Changes in blood pressure and sodium balance were studied in all groups. Under baseline conditions there was no hormonal difference between group I and II. In contrast, the children in group III had a suppressed PRA and a 1.5–2 fold elevation of aldo and DOC. Plasma DOC and urinary THDOC increased continuously 10–50 fold in all groups during the ACTH test. Aldo rose transiently 2–4 fold on the first day of ACTH and fell subsequently below baseline levels in group I and II. The children with DSH (group III), however, showed an unusual, sustained aldo stimulation with ACTH. PRA decreased significantly after ACTH in group I and II. Sodium retention and an elevation of blood pressure were found in all groups during ACTH administration. The highest blood pressure rise was observed in group III (from 124/72 to 139/90 mm Hg). The blood pressure response to ACTH was partly sodium dependent. Although aldo and DOC and sodium retention may contribute to the ACTH induced blood pressure elevation, other factors must play a role.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

References

  1. Abraham, G.E., Buster, J.E., Lucas, L.A., Corrales, P.C., Teller, R.C.: Chromatographic separation of steroid hormones for use in radioimmunoassay. Analyt. Lett.5, 509–517 (1972)

    Google Scholar 

  2. August, J.T., Nelson, D.H., Thorn, G.W.: Response of normal subjects to large amounts of aldosterone. J. Clin. Invest.37, 1549–1555 (1958)

    Google Scholar 

  3. August, J.T., Nelson, D.H.: Adjustment to aldosterone or desoxycorticosterone acetate induced sodium retention in patients with Addison's disease. J. Clin. Invest.38, 1964–1971 (1959)

    Google Scholar 

  4. Biglieri, E.G., Slaton, P.E. Jr., Schambelan, M., Kronfield, S.J.: Hypermineralocorticoidism. Am. J. Med.45, 170–175 (1968)

    Google Scholar 

  5. Biglieri, E.G., Schambelan, M., Slaton, P.E. Jr.: Effect of adrenocorticotropin on desoxycorticosterone, corticosterone and aldosterone excretion. J. Clin. Endocrinol. Metab.29, 1090–1101 (1969)

    Google Scholar 

  6. Biglieri, E.G.: Plasma desoxycorticosterone concentrations in the adrenal enzymatic deficiencies causing hypertension. In: Juvenile Hypertension, Kroc Foundation Series, Vol. 8. M.I. New, L.S. Levine (eds.), pp. 171–176. New York, Raven Press 1977

    Google Scholar 

  7. Brown, R.D., Strott, C.A.: Plasma deoxycorticosterone in man. Clin. Endocrinol. Metab.32, 744–750 (1971)

    Google Scholar 

  8. Conn, J.W.: I. Painting background. II. Primary aldosteronism, a new clinical syndrome. J. Lab. Clin. Med.45, 3–17 (1955)

    Google Scholar 

  9. Dawborn, J.K.: The effect of prolonged intravenous infusion of aldosterone in a normal human subject. Med. J. Australia1, 1079–1083 (1969)

    Google Scholar 

  10. deNicola, A.F., de la Riva, I.J., Basso, N., Dahl, V., Kaplan, S.: Effects of ACTH and salt on blood pressure and steroid secretion in rats. Acta Physiol. Lat. Am.22, 231–240 (1972)

    Google Scholar 

  11. Fan, J.S.K., Coghlan, J.P., Denton, D.A., Oddie, C.A., Scoggins, B.A., Shulkes, A.A.: Effect of intravenous infusion of corticosteroids on blood pressure, electrolytes, and water metabolism in sheep. Am. J. Physiol.228, 1695–1701 (1975)

    Google Scholar 

  12. Ganong, W.F.: Effect of sympathetic activity and ACTH on renin and aldosterone secretion. In: Hypertension '72, J. Genest and E. Koiw (eds.), pp. 4–14. Berlin-Heidelberg-New York: Springer 1972

    Google Scholar 

  13. Giebink, G.S., Gotlin, R.W., Biglieri, E.G., Katz, F.A.: A kindred with familial glucocorticoid-suppressible aldosteronism. J. Clin. Endocrinol. Metab.36, 715–723 (1973)

    Google Scholar 

  14. Grim, C.E., Weinberger, M.H., Anand, S.K., Northway, J.D.: Familial, normokalemic, glucocorticoid-suppressible hyperaldosteronism. Clin. Res.22, 632A (1974)

  15. Hoefnagles, W.H.L., Hofman, J.A., Smals, A.G.H., Drayer, J.I.M., Kloppenborg, J.W.C., Benraad, Th.J.: Dexamethasone-responsive hypertension in young women with suppressed renin and aldosterone. LancetI, 741–743 (1978)

    Google Scholar 

  16. Honda, M., Nowaczynski, W., Messerli, F., Kuchel, O., Genest, J.: Plasma deoxycorticosterone and aldosterone in essential hypertension. J. Steroid Biochem.7, 565–569 (1976)

    Google Scholar 

  17. Kaplan, N.M., Bartter, F.C.: The effect of ACTH, renin, angiotensin II, and various precursors on biosynthesis of aldosterone by adrenal slices. J. Clin. Invest.41, 715–724 (1962)

    Google Scholar 

  18. McCaa, R.E.: Aldosterone and arterial blood pressure response to long-term infusion of adrenocorticotropic hormone (ACTH) in conscious dogs during sodium repletion and sodium depletion. Fed. Proc.37, 811 (1978)

    Google Scholar 

  19. Miura, K., Yoshinaga, K., Goto, K., Katsushima, I., Maebashi, M., Demura, H., Iino, M., Demura, R., Torikai, T.: A case of glucocorticoid-responsive hyperaldosteronism. J. Clin. Endocrinol. Metab.28, 1807–1815 (1968)

    Google Scholar 

  20. Mok, M., Gless, K.H., Vecsei, P.: Tetrahydrodeoxycorticosterone radioimmunoassay in human urine after chromatography. Acta Endocrinol. 84, Suppl.208, 115–116 (1977)

    Google Scholar 

  21. New, M.I., Peterson, R.E.: A new form of congenital adrenal hyperplasia. J. Clin. Endocrinol. Metab.27, 300–305 (1967)

    Google Scholar 

  22. New, M.I., Siegal, E., Peterson, R.E.: Dexamethasone-suppressible hyperaldosteronism. J. Clin. Endocrinol. Metab.37, 93–100 (1973)

    Google Scholar 

  23. New, M.I., Peterson, R.E., Saenger, P., Levine, L.S.: Evidence for an unidentified ACTH-induced steroid hormone causing hypertension. J. Clin. Endocrinol. Metab.43, 1283–1293 (1976)

    Google Scholar 

  24. Newton, M.A., Laragh, J.H.: Effect of corticotropin on aldosterone excretion and plasma renin in normal subjects, in essential hypertension and in primary aldosteronism. J. Clin. Endocrinol. Metab.28, 1006–1013 (1968)

    Google Scholar 

  25. Nowaczynski, W., Kuchel, O., Genest, J.: Aldosterone, deoxycorticosterone, and corticosterone metabolism in benign hypertension. In: Hypertension '72. J. Genest and E. Koiw (eds.), pp. 244–255. Berlin-Heidelberg-New York: Springer 1972

    Google Scholar 

  26. Oddie, C., Coghlan, J., Scoggins, B.: Plasma deoxycorticosterone levels in man with simultaneous measurement of aldosterone, corticosterone, cortisol and 11-deoxycortisol. J. Clin. Endocrinol. Metab.34, 1039–1054 (1972)

    Google Scholar 

  27. Perera, G.A.: Modification of blood pressure by cortisone and ACTH in normotensives and hypertensives. Proc. of the First Clinical ACTH Conference 284 (1950)

  28. Pratt, J.H., Dale, S.L., Melby, J.C.: The effect of administered ACTH on aldosterone metabolism and secretion. J. Clin. Endocrinol. Metab..42, 355–360 (1976)

    Google Scholar 

  29. Ragan, C.: Corticotropin, cortisone and related steroids in clinical medicine: Practical considerations. Bull. N.Y. Acad. Med.29, 355–376 (1953)

    Google Scholar 

  30. Rauh, W., Levine, L.S., Forster, E., New, M.I.: Aldosterone metabolism after prolonged ACTH administration in juvenile hypertension. Pediatr. Res.12, 156 (1978)

    Google Scholar 

  31. Rosemberg, E., Demany, M., Budnitz, E., Underwood, R., Leard, A., Leard, R.S.: Effects of administration of large amounts of d-aldosterone in normal subjects and in a patient with Sheenan's syndrome. J. Clin. Endocrinol. Metab.22, 465–480 (1962)

    Google Scholar 

  32. Ross, E.J., Hurst, P.E.: Effect of prolonged administration of aldosterone and corticosterone on plasma and urinary electrolytes in man. Clin. Sci. Mol. Med.28, 91–98 (1965)

    Google Scholar 

  33. Schömig, A., Lüth, B., Dietz, R., Gross, F.: Changes in vascular smooth muscle sensitivity to vasoconstrictor agents induced by corticosteroids, adrenalectomy, and differing salt intake in rats. Clin. Sci. Mol. Med.51, 61s-63s (1976)

    Google Scholar 

  34. Scoggins, B.A., Coghlan, C.P., Denton, D.A., Fan, J.S.K., McDougall, J.G., Oddie, C.J., Shulkes, A.A.: Metabolic effects of ACTH in the sheep. Am. J. Physiol.266, 198–205 (1974)

    Google Scholar 

  35. Scoggins, B.A., Coghlan, J.P., Denton, D.A., Fan, J.S., McDougall, J.G.: Mechanism of ACTH induced hypertension. In: Program and Abstracts—58th Annual Meeting. The Endocrine Society. San Francisco, California (Abstract No. 211)

  36. Sealey, J.E., Laragh, J.H.: Radioimmunoassay of plasma renin activity. Semin. Nucl. Med.5, 189–202 (1975)

    Google Scholar 

  37. Tan, D.Y., Noth, R.H., Mulrow, P.J.: The role of 11-deoxycorticosterone in human hypertension. Clin. Sci. Mol. Med.51, 311s-314s (1976)

    Google Scholar 

  38. Vecsei, P., Kessler, H.: In vivo conversion of corticosterone into aldosterone in rats treated with ACTH or submitted to stress. Experientia26, 1015–1016 (1970)

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Rauh, W., Levine, L.S., Gottesdiener, K. et al. Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension. Klin Wochenschr 56 (Suppl 1), 161–167 (1978). https://doi.org/10.1007/BF01477468

Download citation

  • Received:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01477468

Schlüsselwörter

Key words

Navigation