Short-term growth hormone excess increased angiotensin II levels (205.9 vs 117.5 pMol/L; p=0.03), while long-term excess in acromegaly patients decreased them compared to controls (p=0.017).
Observational (n=54)
Does short- and long-term growth hormone excess alter renin-angiotensin system activity?
Short-term growth hormone excess stimulates the renin-angiotensin system, whereas long-term excess in acromegaly down-regulates it despite higher blood pressure.
p-value: p=0.03
Abstract Background The renin-angiotensin system (RAS) constitutes an important cornerstone in blood pressure (BP) regulation. Previous evidence on the relationship between growth hormone (GH), insulin-like growth factor I (IGF-I), and the RAS is conflicting, depending on study conditions and exposure duration. This exploratory study therefore investigated the effects of short- and long-term GH excess on RAS activity. Methods RAS activity was assessed in 10 healthy, male volunteers (26±5years, BMI 23±3.4kg/m2) before and after one week of daily, subcutaneous GH treatment (2mg) serving as model of short-term GH excess. Regarding long-term GH excess, RAS activity in 19 patients with active acromegaly (5448-59years, 52.6% females, IGF-I/ULN 2.82.3-3.3) was compared to a cohort of 25 controls (3932-47years, 76% females). In 12 patients, measurements were re-conducted after successful treatment of acromegaly. Results One week of GH treatment increased IGF-I concentrations to 1.6±0.5 ULN and overall RAS activity, including angiotensin II levels (117.5 ±50.3pMol/L vs. 205.9 ±135.7pMol/L, p=0.03) and the surrogate of renin activity (PRA-S: 149.8 ±63.3pMol/L vs. 269.1 ±177.4pMol/L, p=0.03) alongside increased concentrations of insulin and C-peptide in healthy males. In contrast, patients with acromegaly showed lower concentrations of angiotensin II (47.233-145pMol/L vs. 155.364-326pMol/L, p=0.017), aldosterone (11871-193pMol/L vs. 227.8165-305pMol/L, p=0.009), and PRA-S(84.251-200pMol/L vs. 23085-403pMol/L, p=0.032) despite higher mean arterial BP(10599-115mmHg vs. 9185-97mmHg, p 0.001) compared to controls. 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.
Baumgartner et al. (Tue,) conducted a observational in Growth hormone excess and Acromegaly (n=54). Growth hormone excess (short-term treatment and long-term acromegaly) vs. Baseline and healthy controls was evaluated on Renin-angiotensin system activity including angiotensin II levels (p=0.03). Short-term growth hormone excess increased angiotensin II levels (205.9 vs 117.5 pMol/L; p=0.03), while long-term excess in acromegaly patients decreased them compared to controls (p=0.017).