Hansen T K, Møller J, Thomsen K, Frandsen E, Dall R, Jørgensen J O, Christiansen J S
Medical Department M (Endocrinology and Diabetes), Institute for Basic Psychiatric Research, Aarhus University Hospital, DK-8000 Aarhus C, Denmark.
Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1326-32. doi: 10.1152/ajpendo.2001.281.6.E1326.
To investigate the mechanisms behind the water- and sodium-retaining effects of growth hormone (GH), we studied the effect of GH on 1) water and sodium homeostasis, 2) the renin-angiotensin-aldosterone system (RAAS), and 3) lithium clearance (C(Li)) with and without concomitant prostaglandin (PG) synthesis inhibition with ibuprofen. GH administration for 6 days induced a significant increase in plasma renin, which was abolished by coadministration of ibuprofen (mU x l(-1) x 24 h(-1): control: 22.4 +/- 4.3; GH: 37.7 +/- 8.8; ibuprofen: 15.2 +/- 3.0; GH + ibuprofen: 19.7 +/- 2.5; ANOVA: P < 0.01). Comparable increments in extracellular volume were seen after 6-day treatment with GH alone and in combination with ibuprofen [liters: control, 19.57 +/- 0.92; GH, 20.80 +/- 1.00 (ANOVA: P < 0.0005); ibuprofen, 19.38 +/- 0.90; GH + ibuprofen, 21.63 +/- 1.37 (ANOVA: P < 0.0005)]. Treatment with GH increased C(Li) and changed the tubular handling of sodium and water. The absolute distal sodium reabsorption was increased, and this was only partially counterbalanced by decreased reabsorption in the proximal tubules. The data demonstrate that GH-induced activation of the RAAS can be blocked by concomitant PG synthesis inhibition and that the tubular effects of GH include increased distal nephron sodium and water reabsorption.
