Evidence against prolactin stimulation of aldosterone in normal human subjects and patients with primary aldosteronism, including a patient with primary aldosteronism and a prolactin-producing pituitary microadenoma

O. B. Holland, C. E. Gomez-Sanchez, D. C. Kem, M. H. Weinberger, N. J. Kramer, J. R. Higgins

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

In addition to ACTH, another cranial factor, possibly prolactin, might stimulate aldosterone secretion. To evaluate this possibility, plasma prolactin concentration was determined in normal subjects and patients with primary aldosteronism during regular sodium diet and low sodium diet and was correlated with plasma aldosterone and cortisol concentration during 0200-0800 h circadian rhythm studies with plasma samples obtained every 20 min. Plasma prolactin and aldosterone concentrations exhibited a positive correlation in only one of three normal subjects during regular sodium diet and in two of four patients with primary aldosteronism during dexamethasone administration. Plasma prolactin and cortisol concentrations correlated positively with a similar frequency. Dexamethasone administration suppressed plasma prolactin concentration in three normal subjects and three of four patients with primary aldosteronism during regular sodium diet and one of two normal subjects during low sodium diet. Plasma prolactin concentration did not change with low sodium diet, saline infusion, or upright posture in normal subjects and patients with primary aldosteronism. One patient with primary aldosteronism (bilateral hyperplasia) was found to have a prolactin-producing microadenoma. During prolactin stimulation with TRH and suppression with L-dopa, plasma aldosterone concentration did not similarly change. Transsphenoidal removal of the microadenoma did not affect the primary aldosteronism. Mean plasma prolactin concentration in patients with primary aldosteronism due to bilateral zona glomerulosa hyperplasia (13 patients) was not different from that in patients with primary aldosteronism due to an adenoma (15 patients) or from that in normal subjects. Thus, prolactin does not appear to stimulate aldosterone in normal human subjects and in patients with primary aldosteronism. In addition, the lack of change in plasma prolactin concentration with low sodium diet and saline infusion casts some doubt upon its relevance in sodium and water metabolism in man.

Original languageEnglish (US)
Pages (from-to)1064-1076
Number of pages13
JournalJournal of Clinical Endocrinology and Metabolism
Volume45
Issue number5
StatePublished - 1977

Fingerprint

Hyperaldosteronism
Aldosterone
Prolactin
Nutrition
Plasmas
Sodium
Sodium-Restricted Diet
Dexamethasone
Hyperplasia
Hydrocortisone
Diet
Zona Glomerulosa
Levodopa
Circadian Rhythm
Posture
Metabolism
Adenoma
Adrenocorticotropic Hormone

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Evidence against prolactin stimulation of aldosterone in normal human subjects and patients with primary aldosteronism, including a patient with primary aldosteronism and a prolactin-producing pituitary microadenoma. / Holland, O. B.; Gomez-Sanchez, C. E.; Kem, D. C.; Weinberger, M. H.; Kramer, N. J.; Higgins, J. R.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 45, No. 5, 1977, p. 1064-1076.

Research output: Contribution to journalArticle

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abstract = "In addition to ACTH, another cranial factor, possibly prolactin, might stimulate aldosterone secretion. To evaluate this possibility, plasma prolactin concentration was determined in normal subjects and patients with primary aldosteronism during regular sodium diet and low sodium diet and was correlated with plasma aldosterone and cortisol concentration during 0200-0800 h circadian rhythm studies with plasma samples obtained every 20 min. Plasma prolactin and aldosterone concentrations exhibited a positive correlation in only one of three normal subjects during regular sodium diet and in two of four patients with primary aldosteronism during dexamethasone administration. Plasma prolactin and cortisol concentrations correlated positively with a similar frequency. Dexamethasone administration suppressed plasma prolactin concentration in three normal subjects and three of four patients with primary aldosteronism during regular sodium diet and one of two normal subjects during low sodium diet. Plasma prolactin concentration did not change with low sodium diet, saline infusion, or upright posture in normal subjects and patients with primary aldosteronism. One patient with primary aldosteronism (bilateral hyperplasia) was found to have a prolactin-producing microadenoma. During prolactin stimulation with TRH and suppression with L-dopa, plasma aldosterone concentration did not similarly change. Transsphenoidal removal of the microadenoma did not affect the primary aldosteronism. Mean plasma prolactin concentration in patients with primary aldosteronism due to bilateral zona glomerulosa hyperplasia (13 patients) was not different from that in patients with primary aldosteronism due to an adenoma (15 patients) or from that in normal subjects. Thus, prolactin does not appear to stimulate aldosterone in normal human subjects and in patients with primary aldosteronism. In addition, the lack of change in plasma prolactin concentration with low sodium diet and saline infusion casts some doubt upon its relevance in sodium and water metabolism in man.",
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AU - Holland, O. B.

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AU - Kramer, N. J.

AU - Higgins, J. R.

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