Oxytocin polyuria and polydipsia is blocked by NaCl administration in food-deprived male rats.
Summary of "Oxytocin polyuria and polydipsia is blocked by NaCl administration in food-deprived male rats."
ABSTRACT We examined the effects of NaCl injections on the polydipsia and polyuria induced by subcutaneous oxytocin (OT) administration in food-deprived male rats. During the first 12 hours of the treatment day, both food deprivation and OT administration increased urine excretion but reduced water intake, water balance (fluid intake minus urine volume), and body weight. In fact, OT treatment enhanced the urine excretion and the reduction in water balance and body weight without reducing the water intake of food-deprived animals. Analysis of the physiological effects of OT administration showed increases in urinary sodium concentration, sodium excretion and a reduced plasma sodium concentration. During the second 12 hours, OT increased both urine excretion and water intake in food-deprived but not in ad lib-fed rats. However, hypertonic NaCl administration at the start of this second 12 h period blocked the polyuric and polydipsic responses observed in the OT/deprived group but increased the water intake of ad lib groups. After the whole 24 h period, animals treated with OT showed a water balance and body weight change matching those observed in Control animals. Although the recording time period is a critical factor to demonstrate the effect of peripheral OT administration on water intake, these results suggest that the polyuric and polydipsic responses observed in food-deprived animals depend on the negative sodium and water balance induced by the natriuretic effect of OT and the unavailability of sodium. These OT-induced deficits can be counteracted by the administration of hypertonic NaCl solutions or simply by the intake of standard food.
.Psychobiology, University of Granada, Granada 18071, Spain.
This article was published in the following journal.
Name: Journal of neuroendocrinology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20649851
- DOI: http://dx.doi.org/10.1111/j.1365-2826.2010.02050.x
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Medical and Biotech [MESH] Definitions
Cell surface proteins that bind oxytocin with high affinity and trigger intracellular changes which influence the behavior of cells. Oxytocin receptors in the uterus and the mammary glands mediate the hormone's stimulation of contraction and milk ejection. The presence of oxytocin and oxytocin receptors in neurons of the brain probably reflects an additional role as a neurotransmitter.
A condition due to decreased dietary intake of potassium, as in starvation or failure to administer in intravenous solutions, or to gastrointestinal loss in diarrhea, chronic laxative abuse, vomiting, gastric suction, or bowel diversion. Severe potassium deficiency may produce muscular weakness and lead to paralysis and respiratory failure. Muscular malfunction may result in hypoventilation, paralytic ileus, hypotension, muscle twitches, tetany, and rhabomyolysis. Nephropathy from potassium deficit impairs the concentrating mechanism, producing polyuria and decreased maximal urinary concentrating ability with secondary polydipsia. (Merck Manual, 16th ed)
A nonapeptide hormone released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). It differs from VASOPRESSIN by two amino acids at residues 3 and 8. Oxytocin acts on SMOOTH MUSCLE CELLS, such as causing UTERINE CONTRACTIONS and MILK EJECTION.
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