GH and water retention?
- Thread starter Mr.50
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jcam222
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I have never seen anyone post the answer to this so look forward to seeing thoughts. I have often seen people post that water retention is a side but never seen the mechanism. I am on low dose and believe I am having water retention in the stomach and face which I hate with a passion.
aequitas
New member
GH causes sodium and potassium retention. Sodium and potassium secrection is reduced by an action independent of the adrenal glands. The reason is still debated, but most physiology and endocrinology textbooks state that it is probably because sodium and potassium are diverted from the kidneys to the growing tissues.
Mr.50
Board Supporter
SO if it was intra lean tissue potassium retention it should add only water retention to in inside of tissues giving you fullness (simplification). While I agree this is what most of the books say I does not account for the reports of sub-Q water retention. Is there any truth to what Glenihan said, meaning if I went with sub-q inj in thigh instead of abdomen would that reduce water rretention in abs (even if it decreases inj site fat loss).
Mr.50
Mr.50
aequitas
New member
An interesting study.................
GH increases extracellular volume by stimulating sodium reabsorption in the distal nephron and preventing pressure natriuresis.
Johannsson G, Sverrisdottir YB, Ellegard L, Lundberg PA, Herlitz H.
Research Center for Endocrinology and Metabolism, Department of Clinical Neurophysiology, Sahlgrenska University Hospital, Goteborg SE-413 45, Sweden. [email protected]
Although sodium retention and volume expansion occur during GH administration, blood pressure is decreased or unchanged. The aim was to study the effect of short- and long-term GH replacement in adults on sodium balance, renal hemodynamics, and blood pressure. Ten adults with severe GH deficiency were included into a 7-d, randomized, placebo-controlled, cross-over trial followed by 12 months of open GH replacement. All measurements were performed under metabolic ward conditions. Extracellular water (ECW) was determined using multifrequency bioelectrical impedance analysis. Renal plasma flow and glomerular filtration rate were assessed using renal paraminohippurate and Cr(51) EDTA clearances, respectively. Renal tubular sodium reabsorption was assessed using lithium clearance. Plasma renin activity (PRA), plasma concentrations of angiotensin II, aldosterone, atrial natriuretic peptides and brain natriuretic peptides (BNP) and 24-h urinary norepinephrine excretion were measured. Seven days of GH treatment decreased urinary sodium excretion. Lithium clearance as a marker of proximal renal tubular sodium reabsorption was unaffected by GH treatment. ECW was increased after both short- and long-term treatment. This increase was inversely correlated to the decrease in diastolic blood pressure (r = -0.70, P = 0.02) between baseline and 12 months. Short-term treatment increased PRA and decreased BNP. The increase in PRA correlated with an increase in 24-h urinary norepinephrine excretion (r = 0.77, P < 0.01). Glomerular filtration rate and renal plasma flow did not change during treatment. The sodium- and water-retaining effect of GH takes place in the distal nephron. The sustained increase in ECW in response to GH is associated with an unchanged or decreased blood pressure. This together with unchanged or decreased atrial natriuretic peptides and BNP may prevent pressure-induced escape of sodium.
GH increases extracellular volume by stimulating sodium reabsorption in the distal nephron and preventing pressure natriuresis.
Johannsson G, Sverrisdottir YB, Ellegard L, Lundberg PA, Herlitz H.
Research Center for Endocrinology and Metabolism, Department of Clinical Neurophysiology, Sahlgrenska University Hospital, Goteborg SE-413 45, Sweden. [email protected]
Although sodium retention and volume expansion occur during GH administration, blood pressure is decreased or unchanged. The aim was to study the effect of short- and long-term GH replacement in adults on sodium balance, renal hemodynamics, and blood pressure. Ten adults with severe GH deficiency were included into a 7-d, randomized, placebo-controlled, cross-over trial followed by 12 months of open GH replacement. All measurements were performed under metabolic ward conditions. Extracellular water (ECW) was determined using multifrequency bioelectrical impedance analysis. Renal plasma flow and glomerular filtration rate were assessed using renal paraminohippurate and Cr(51) EDTA clearances, respectively. Renal tubular sodium reabsorption was assessed using lithium clearance. Plasma renin activity (PRA), plasma concentrations of angiotensin II, aldosterone, atrial natriuretic peptides and brain natriuretic peptides (BNP) and 24-h urinary norepinephrine excretion were measured. Seven days of GH treatment decreased urinary sodium excretion. Lithium clearance as a marker of proximal renal tubular sodium reabsorption was unaffected by GH treatment. ECW was increased after both short- and long-term treatment. This increase was inversely correlated to the decrease in diastolic blood pressure (r = -0.70, P = 0.02) between baseline and 12 months. Short-term treatment increased PRA and decreased BNP. The increase in PRA correlated with an increase in 24-h urinary norepinephrine excretion (r = 0.77, P < 0.01). Glomerular filtration rate and renal plasma flow did not change during treatment. The sodium- and water-retaining effect of GH takes place in the distal nephron. The sustained increase in ECW in response to GH is associated with an unchanged or decreased blood pressure. This together with unchanged or decreased atrial natriuretic peptides and BNP may prevent pressure-induced escape of sodium.
aequitas
New member
Atrial natriuretic peptide is released by the atria of the heart in response to increased blood volume. ANP promotes natriuresis, which is elevated urinary excretion of sodium and chloride, which decreases blood volume. GH inhibiting this explains the extracellular water retention. It does seem as though changing the injection site would help with site-specific responses, but there will always be this systematic response. As far as any ways to combat this......i would say lower your sodium intake slightly and always drink plenty of water, or either just tough it out.