Why the study?
Does central inactivation of oxytocin or ANP receptors alter the osmotic inhibition of hypovolemia-induced salt appetite in rats?
Does central inactivation of oxytocin or ANP receptors alter the osmotic inhibition of hypovolemia-induced salt appetite in rats?
Central ANP receptors mediate both sodium- and osmolality-induced inhibition of salt appetite, whereas central oxytocin receptors primarily mediate osmolality-induced inhibition in rats.
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Central ANP/oxytocin receptor inactivation may alter osmotic salt appetite control in rats; hypothesis-generating and leaves open translational relevance to human volume homeostasis.
These studies evaluated the involvement of central oxytocin (OT) and atrial natriuretic peptide (ANP) receptors in the osmotic inhibition of hypovolemia-induced salt appetite. Rats were pretreated centrally with the A chain of the cytotoxin ricin conjugated to OT (rAOT) or ANP (rAANP) to selectively inactivate cells bearing these respective receptors, or rats were pretreated with the unconjugated A chain (rA) as a control. Hypovolemia was induced with subcutaneous colloid injections, and rats then were given either 2 M mannitol, which raises plasma osmolality but lowers plasma sodium, or 1 M NaCl, which raises both. Hypertonic mannitol inhibited saline ingestion in rA-treated control rats but stimulated ingestion in rAOT- and rAANP-treated rats, whereas hypertonic NaCl blunted saline ingestion in rA- and rAOT-treated rats but stimulated ingestion in rAANP-treated rats. Angiotensin II-induced saline intake was similarly potentiated in rAOT- and rAANP-treated rats, indicating that this treatment also activates central inhibitory OT and ANP pathways. These data suggest that central ANP receptors mediate both Na(+)- and osmolality-induced inhibition of NaCl ingestion, whereas central OT receptors primarily mediate osmolality-induced inhibition of NaCl ingestion in rats.
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Blackburn et al. (1995) studied this question.
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