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PMID:19723921

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Citation

White, MM and Samson, WK (2009) A possible relationship between brain-derived adrenomedullin and oxytocin in the regulation of sodium balance. J. Endocrinol. 203:253-62

Abstract

Exaggerated thirst and salt appetite occurs when endogenous, brain-derived adrenomedullin (AM) production is compromised. In addition, the arginine vasopressin (AVP) response to hypovolemia is compromised. We hypothesized that AM acts in the hypothalamus to control oxytocin (OT) release and that the inhibitory action of AM on salt appetite is mediated via its effects on OT release in the rat. When plasma tonicity was elevated with sodium, ribozyme-induced compromise of central AM production significantly blunted the release of OT into plasma. OT responses to elevation of plasma osmolality without concomitant change in plasma sodium levels were not altered by compromise of AM production. Thus, brain-derived AM controls OT release in response to altered plasma sodium levels. Furthermore, central AM-induced inhibition of NaCl intake can be reversed by pretreatment with an OT antagonist, and the increase in NaCl appetite seen following ribozyme compromise of central AM can be attenuated with central OT administration. These data support the hypothesis that endogenous, brain-derived AM is an essential participant in the hypothalamic response to hypernatremia via its actions on OT-expressing neurons. Together with our previous reports of the effects of AM on AVP secretion and ingestive behaviors, our results suggest that endogenous AM is a physiologically relevant regulator of the endocrine and behavioral mechanisms that maintain fluid and electrolyte homeostasis.

Links

PubMed Online version:10.1677/JOE-09-0284

Keywords

Adrenomedullin/physiology; Animals; Arginine Vasopressin/blood; Brain/physiology; Male; Oxytocin/blood; Oxytocin/physiology; Polyethylene Glycols/pharmacology; RNA, Catalytic/pharmacology; Rats; Rats, Sprague-Dawley; Sodium/metabolism; Sodium, Dietary/administration & dosage

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

RAT:ADML

involved_in

GO:0046879: hormone secretion

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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