Short-term growth hormone (GH) treatment of GH-deficient adults increases body sodium and extracellular water, but not blood pressure.

Short-term rhGH increases PIIINP, a biomarker of endothelial dysfunction

“…Sustained increased plasma levels of IGF-I may predispose an individual to long term ED and may be accounted for by an inverse correlation of NO levels with GH and IGF-I excess [41]. In the present study the effect on HR and RPP which occurred, could be explained by the effects of IGF-I on NO production, impairing baroreceptor function, via activation of the NO-system, elevating HR without affecting BP [42], corroborating similar short-term rhGH administration [39]. The research group had previously identified a significant reduction of independent cardiovascular risk factors, following rhGH administration, without an identification of changes in PIIINP [43].…”

“…The significantly decreased lower limb pre-occlusion APW velocity in the rhGH group is comparable with the effects of rhGH on endothelial dysfunction (ED) in growth hormone deficiency (GHD) [14] and in heart failure [15]. The most common short term effects following rhGH administration are from sodium and water retention and weight gain, from dependent oedema, which can frequently occur within days [39]. It does this in GHD [39] and in healthy subjects by activation of the renin-angiotensin system, increasing aldosterone secretion, by inhibiting atrial natriuretic peptide secretion and by a direct action on renal tubules [40].…”

“…The most common short term effects following rhGH administration are from sodium and water retention and weight gain, from dependent oedema, which can frequently occur within days [39]. It does this in GHD [39] and in healthy subjects by activation of the renin-angiotensin system, increasing aldosterone secretion, by inhibiting atrial natriuretic peptide secretion and by a direct action on renal tubules [40]. In the present study, the sodium level was significantly increased, but remained within the normal reference range, but this may have accounted for the elevation in resting HR and RPP, which occurs in acromegaly.…”

Growth hormone regulation of glomerular AT1angiotensin receptors in adult uninephrectomized male rats

“…These data suggest that circulating GH mediates in vivo remnant kidney growth by modulating AT 1 R binding sites. The concept that GH interacts with the reninangiotensin system is new (9) and has been substantiated only within the last decade (2,10,14,30). However, the mechanisms by which GH and ANG II regulate each other's secretion are not clear (3,14).…”

Is growth hormone deficiency contributing to heart failure in patients with beta-thalassemia major?

“…At admission, the patient had for several months been treated with enalapril, spironolactone, digoxin, furosemide and DFO, but her heart failure progressed. Fluid retention with increase in extracellular water is an acute effect of GH treatment but seems to be physiological and does not affect blood pressure (27). In the state of the extreme heart failure, the infusion rate of diuretics was kept at a high level to allow a continuous diuresis of 2 -300 ml per h.…”