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Expansion of Extracellular Volume and Suppression of Atrial Natriuretic Peptide after Growth Hormone Administration in Normal Man

University Department of Endocrinology and Internal Medicine and Department of Medicine and Nephrology C., Aarhus Kommunehospital DK 8000 Aarhus, Denmark.

Address correspondence and requests for reprints to: Jens Møller, Medical Department M, Aarhus Kommunehospital, DK 8000 Aarhus, Denmark.

Sodium retention and symptoms and signs of fluid retention are commonly recorded during GH administration in both GH-deficient patients and normal subjects. Most reports have however, been casuistic or uncontrolled. In a randomized double blind placebo-controlled cross-over study we therefore examined the effect of 14-day GH administration (12 IU sc at 2000 h) on plasma volume, extracellular volume (ECV), atrial natriuretic peptide (ANP), arginine vasopressin, and the renin angiotensin system in eight healthy adult men. A significant GH induced increase in serum insulin growth factor I was observed. GH caused a significant increase in ECV (L): 20.45 ± 0.45 (GH), 19.53 ± 0.48 (placebo) (P < 0.01), whereas plasma volume (L) remained unchanged 3.92 ± 0.16 (GH), 4.02 ± 0.13 (placebo). A significant decrease in plasma ANP (pmol/L) after GH administration was observed: 2.28 ± 0.54 (GH), 3.16 ± 0.53 (placebo) P < 0.01. Plasma aldosterone (pmol/L): 129 ± 14 (GH), 89 ± 17 (placebo), P = 0.08, and plasma angiotensin II (pmol/L) levels: 18 ± 12 (GH), 14 ± 7 (placebo), P = 0.21, were not significantly elevated. No changes in plasma arginine vasopressin occurred (1.86 ± 0.05 pmol/L vs. 1.90 ± 0.05, P = 0.33). Serum sodium and blood pressure remained unaffected. Moderate complaints, which could be ascribed to water retention, were recorded in four subjects [periorbital edema (n = 3), acral paraesthesia (n = 2) and light articular pain (n = 1)]. The symptoms were most pronounced after 2–3 days of treatment and diminished at the end of the period. In summary, 14 days of high dose GH administration caused a significant increase in ECV and a significant suppression of ANP. (J Clin Endocrinol Metab 72: 768–772, 1991)

Received July 31, 1990.

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