This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints, Permissions and Rights Citing Articles Citing Articles via Google Scholar Google Scholar Articles by BRICKMAN, A. S. Articles by TUCK, M. L. Search for Related Content PubMed PubMed Citation Articles by BRICKMAN, A. S. Articles by TUCK, M. L.

Diminished Aldosterone Responses to Angiotensin II and Adrenocorticotropin in Hypocalcemic Subjects: Restoration of Responsiveness with Normocalcemia

UCLA School of Medicine Los Angeles, California 90024
The Veterans Administration Medical Center Sepulueda, California 91343

Address requests for reprints to: Arnold S. Brickman, M.D., Mineral Metabolism (HIE), Veterans Administration Medical Center, Sepulveda, California 91343.

ACTH-, angiotensin II (All)-, and K⁺-mediated aldosterone responses in vitro are dependent on extracellular and intracellular Ca concentrations. This study examined in vivo the relationship of changes in ambient serum calcium (serum Ca) to ACTH- and AH-mediated aldosterone release in hypoparathyroid subjects. Plasma aldosterone (PA) responses to graded dose infusions of ACTH and AH were examined in hypoparathyroid (HypoPTH) patients before (n = 8) and after correction of hypocalcemia (n = 6) and compared to responses in 20 normotensive normocalcemic subjects. ACTH and All were infused for 90 min at rates increasing from 12.5 to 50 mIU/ 30 min and 0.5 to 2.0 ng/kg·min, respectively. Pretreatment mean serum Ca was 6.8 ± 0.2 (±SEM) mg/dl, and it rose to 9.3 ± 0.2 mg/dl after 3–8 weeks of vitamin D administration. In the untreated HypoPTH patients, basal mean PA (5.4 ±1.3 ng/dl) was lower (P < 0.01) than in the normal subjects (10.6 ±0.6 ng/ dl) or treated HypoPTH patients (9.5 ± 1.8 ng/dl). There was a marked reduction in PA responses to ACTH at all doses in the untreated HypoPTH patients compared to the normal subjects. With normalization of serum Ca in four patients, the mean peak PA response to ACTH (25.1 ± 6.0 ng/dl) was not significantly different from normal (28.9 ± 1.7 ng/dl). During graded dose AH infusion in five untreated HypoPTH patients, mean PA levels increased from 6.9 ± 1.2 to 11.6 ± 2.2 ng/dl; when the serum Ca was normal, the corresponding values were 8.7 ±1.8 and 20.2 ± 3.61 ng/dl. There was a positive correlation (r = 0.475; P < 0.05) between basal PA and serum Ca levels. In addition, maximum changes in mean arterial pressure in response to All infusions were significantly greater after correction of hypocalcemia. These observations indicate that in HypoPTH patients, extracellular Ca concentrations can influence humoral aldosterone response to ACTH and All and pressor responses to All.

Received March 24, 1986.