Acute and chronic effects of growth hormone on renal regulation of electrolyte and water homeostasis.
until further notice
SourceGrowth Hormone & Igf Research, 17, 5, (2007), pp. 353-368
Article / Letter to editor
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Growth Hormone & Igf Research
SubjectUMCN 5.4: Renal disorders
For decades, growth hormone (GH) has been known to influence electrolyte and water handling in humans and animals. However, the molecular mechanisms underlying the GH-induced anti-natriuretic and anti-diuretic effects have remained elusive. This review will examine the existing literature on renal electrolyte and water handling following acute and chronic GH-exposure. Renal responses to GH differ in acute and chronic models. Acute application of GH results in a reduced urinary electrolyte and water excretion, whereas the chronic effects of GH are more diverse, as this state likely represents a complex mixture of primary and secondary actions of GH as well as compensatory mechanisms. During chronic GH-exposure an initial sodium retaining state often occurs, followed by a normalization of the urinary sodium excretion, although extracellular volume expansion still persists. We recently described a possible mechanism by which GH acutely increases renal electrolyte and water reabsorption, by modulation of the kidney specific Na(+), K(+), 2Cl(-) co-transporter (NKCC2). The primary aim of this review is to investigate how GH-induced regulation of NKCC2 may be involved in the complex renal changes previously described during acute and chronic GH. We propose, that the GH-induced increase in NKCC2 activity may explain the initial water and sodium retention seen in a number of studies. Moreover, renal changes seen during prolonged GH-exposure may now be seen on the background of the acute stimulation of NKCC2. Additionally, GH also promotes renal acidification, thus influencing renal acid/base handling. The GH-induced renal acidification is partly compatible with changes in NKCC2 activity. Finally, we review the available data on changes in hormonal systems affecting tubular transport during acute and chronic GH-exposure.
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