Excretion of electrolytes in Brown Norway and Fischer 344 rats: effects of adrenalectomy and of mineralocorticoid and glucocorticoid receptor ligands.
Experimental Physiology. 2004-10-29; 89(6): 753-765
DOI: 10.1113/expphysiol.2004.028621
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1. Exp Physiol. 2004 Nov;89(6):753-65. Epub 2004 Sep 13.
Excretion of electrolytes in Brown Norway and Fischer 344 rats: effects of
adrenalectomy and of mineralocorticoid and glucocorticoid receptor ligands.
Marissal-Arvy N(1), Mormède P.
Author information:
(1)Neurogénétique et Stress, INSERM U471 – INRA UMR1243 – Université de Bordeaux
2, Institut François Magendie de Neurosciences, 1, rue Camille Saint Saëns, 33077
Bordeaux Cedex, France.
Our previous studies showed that adrenalectomy (ADX) has surprisingly no effect
on body weight and fluid intake in the Brown Norway rat strain, suggesting that
mineralocorticoid receptor (MR)-mediated effects are present even in absence of
corticosteroids in this strain. Moreover, glucocorticoid receptor (GR)-mediated
mechanisms are more effective in Brown Norway than in Fischer 344 rats. Such
functional differences in corticosteroid receptor pathways between Brown Norway
and Fischer 344 rats led us to compare the effect of ADX and MR/GR-mediated
actions on sodium and potassium excretion between these two rat strains. To this
end, we first measured the effect of an acute high dose of aldosterone on the
urinary Na+/K+ concentration ratio in intact and ADX Brown Norway and Fischer 344
rats. Second, to discriminate mineralocorticoid from glucocorticoid actions, we
treated chronically ADX rats with increasing doses of aldosterone or RU28362, a
pure GR agonist, in the drinking fluid. As sodium homeostasis involves salt
appetite regulation, behaviour under mineralocorticoid control, we also measured
saline preference in Brown Norway and Fischer 344 rats. Our data illustrate: (1)
the very limited effect of ADX on body weight, food and fluid intake, diuresis,
natriuresis, kaliuresis and salt appetite in Brown Norway rats, supporting the
presence of MR signalling pathways in the absence of adrenal steroids in these
rats; (2) the insensitivity of MR to aldosterone in intact Brown Norway rats, and
the reduced sensitivity of MR to aldosterone in ADX Brown Norway rats compared
with ADX Fischer 344 rats; and (3) the greater sensitivity of GR-related
mechanisms to RU28362 in Brown Norway than in Fischer 344 rats in terms of body
weight gain and electrolyte excretion. Considering that both MRs and GRs regulate
hypothalamic-pituitary-adrenal axis processes, such functional differences in
corticosteroid receptors could be at the origin, at least partly, of the strain
differences in corticotropic activity/reactivity to stress previously described.
DOI: 10.1113/expphysiol.2004.028621
PMID: 15364879 [Indexed for MEDLINE]