Abstract
AbstractGlucocorticoids, produced in adrenal cortex, exert potent natriuretic and diuretic actions in the kidney. Recently, it has been found that glucocorticoids could upregulate the expression of natriuretic peptide receptor A (NPR-A), the primary receptor of atrial natriuretic peptide, in the hypothalamus of the rat. Consequently, systemic administration of glucocorticoid could block dehydration-induced water intake by activation hypothalamic NPR-A. We describe here glucocorticoids could inhibit sodium intake when administrated systemically in conscious, salt-depleted rats; an effect which was strong and long-lasting. The study provided further evidence for the actions of glucocorticoids on central nervous system, which together with their established renal actions coordinated to normalize extracellular fluid volume.
Highlights
Glucocorticoids, produced in adrenal cortex, exert potent natriuretic and diuretic actions in the kidney
It has been found that glucocorticoids could upregulate the expression of natriuretic peptide receptor A (NPR-A), the primary receptor of atrial natriuretic peptide, in the hypothalamus of the rat
Atrial natriuretic peptide (ANP), a peptide hormone secreted by the heart in response to volume expansion, provides a potent defensive mechanism counterbalancing the salt- and water-retaining actions of the renin–angiotensin–aldosterone system that predominates in terrestrial animals
Summary
Glucocorticoids, produced in adrenal cortex, exert potent natriuretic and diuretic actions in the kidney. Glucocorticoids inhibit sodium depletion-induced salt appetite in rat It has been found that glucocorticoids could upregulate the expression of natriuretic peptide receptor A (NPR-A), the primary receptor of atrial natriuretic peptide, in the hypothalamus of the rat.
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