The renin-angiotensin system is activated by short-term, but repressed by long-term growth hormone excess
Authors' conclusion
Short-term GH excess stimulates RAS activity which may be related to the increase in insulin and C-peptide. In contrast, RAS activity is down-regulated in long-term GH excess despite high BP.
Study context
- Population
- Healthy male volunteers (26 ± 5 years, BMI 23 ± 3.4 kg/m²); patients with active acromegaly (54 [48–59] years, 52.6% females, IGF-I/ULN 2.8 [2.3–3.3]) and controls (39 [32–47] years, 76% females)12 re-measured after treatment
- Participants
- 10 / 10 / 19 / 25
- Exposure
- Short-term growth hormone (GH) excess before vs after; long-term GH excess vs controls
- Healthy males before GHn = 10reference
- Healthy males after GHn = 10
- Acromegalyn = 19
- Controlsn = 25reference
- Outcome
- Renin-angiotensin system (RAS) activity
Methodological detailsinterventional before–after study and cross-sectional comparison with controls
- Interventional before–after study and cross-sectional comparison with controls
Main finding
As reported in the abstract
- Short-term GH: IGF-I concentrations increased to (ULN)
- 1.6 ± 0.5
- Short-term GH: angiotensin II, before vs after (pMol/L)
- 117.5 ± 50.3 vs. 205.9 ± 135.7, P = .03
- Short-term GH: PRA-S, before vs after (pMol/L)
- 149.8 ± 63.3 vs. 269.1 ± 177.4, P = .03
- Acromegaly vs controls: angiotensin II (pMol/L), lower
- 47.2 [33-145] vs. 155.3 [64-326], P = .017
- Acromegaly vs controls: aldosterone (pMol/L), lower
- 118 [71-193] vs. 227.8 [165-305], P = .009
- Acromegaly vs controls: PRA-S (pMol/L), lower
- 84.2 [51-200] vs. 230 [85-403], P = .032
- Acromegaly vs controls: mean arterial blood pressure (BP) (mmHg), higher
- 105 [99-115] vs. 91 [85-97], P < .001
Observational data: associations, not effects.
Original publication
The renin-angiotensin system is activated by short-term, but repressed by long-term growth hormone excess. Eur J Endocrinol. Published 17 June 2026. doi:10.
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