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In the present experiments we examined neurohypophyseal hormone secretion in various models of sodium appetite in rats. Basal plasma levels of oxytocin were found to be low in sodium-deficient adrenalectomized rats and in intact animals treated daily with desoxycorticosterone acetate, both of which groups drank large amounts of NaCl solution, whereas basal plasma levels of arginine vasopressin were neither stimulated nor suppressed. Conversely, sodium appetite consistently was inhibited by treatments that stimulated pituitary oxytocin secretion. However, sodium appetite was not inhibited by administration of exogenous oxytocin, nor was it stimulated by administration of an oxytocin receptor antagonist. These and other results suggest that sodium appetite may be inhibited by activity in the supraoptic and/or paraventricular nuclei, the location of the neurons responsible for the synthesis of oxytocin, and can be stimulated only when activity in those neurons is reduced. Whatever the final neural pathway, our data support the hypothesis that the control of sodium appetite is governed by inhibitory as well as excitatory central mechanisms.
E M Stricker, and
J G Verbalis
January 1997,
Regulatory peptides,
E M Stricker, and
J G Verbalis
January 1979,
Hormone research,
E M Stricker, and
J G Verbalis
February 2008,
Experimental physiology,
E M Stricker, and
J G Verbalis
August 1992,
Journal of neuroendocrinology,
E M Stricker, and
J G Verbalis
October 1999,
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas,
E M Stricker, and
J G Verbalis
August 2010,
Nan fang yi ke da xue xue bao = Journal of Southern Medical University,
E M Stricker, and
J G Verbalis
March 1998,
The American journal of physiology,
E M Stricker, and
J G Verbalis
May 2014,
Peptides,
E M Stricker, and
J G Verbalis
February 1983,
Lancet (London, England),
E M Stricker, and
J G Verbalis
February 1973,
Behavioral biology,
