AJP - Endocrinology and Metabolism, Vol 272, Issue 5 E803-E808, Copyright © 1997 by American Physiological Society
Blockade of the renin-angiotensin-aldosterone system prevents growth hormone-induced fluid retention in humans
J. Moller, N. Moller, E. Frandsen, T. Wolthers, J. O. Jorgensen and J. S. Christiansen
Medical Department M (Endocrinology and Diabetes), University Hospital of Aarhus, Denmark.
To test if the renin-angiotensin-aldosterone system (RAAS) is involved in
growth hormone (GH)-associated fluid retention, we examined the effect of
GH administration in the presence or absence of RAAS blockade at different
levels on body fluid homeostasis. Eight subjects were examined in a
controlled, randomized double-blinded trial. During four 6-day periods they
received subcutaneous GH (6 IU-m-2) or placebo injections and tablets as
follows: 1) placebo and placebo, 2) GH and placebo, 3) GH and captopril,
and 4) GH and spironolactone. GH increased extracellular volume (liters;
placebo 18.87 +/- 0.85; GH + placebo 20.43 +/- 1.01) but this effect was
abolished by captopril (GH + captopril 18.82 +/- 0.67) and spironolactone
(GH + spironolactone 18.99 +/- 0.85). Correspondingly, the GH-induced
reduction in bioimpedance was blocked by captopril and spironolactone.
Plasma renin and angiotensin II concentrations increased during all three
GH treatment regimens, whereas plasma aldosterone was increased only after
GH plus spironolactone. The data demonstrate that GH activates the RAAS and
that blockade of the RAAS by two separate mechanisms prevents fluid
retention normally encountered after GH exposure. These observations
suggest that the RAAS plays a key role in GH-induced regulation of fluid
homeostasis.
