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Am J Physiol Regul Integr Comp Physiol 294: R1760-R1767, 2008. First published April 2, 2008; doi:10.1152/ajpregu.00033.2008
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WATER AND ELECTROLYTE HOMEOSTASIS

Tachykinin neurokinin 3 receptor signaling in cholecystokinin-elicited release of oxytocin and vasopressin

Gwendolen E. Haley and Francis W. Flynn

Graduate Neuroscience Program, University of Wyoming, Laramie, Wyoming

Submitted 17 January 2008 ; accepted in final form 30 March 2008

Neurokinin 3 receptor (NK3R) signaling has an integral role in the stimulated oxytocin (OT) and vasopressin (VP) release in response to hyperosmolarity and hypotension. Peripheral injections of cholecystokinin (CCK) receptor agonists for the CCK-A (sulfated CCK-8) and CCK-B (nonsulfated CCK-8) receptors elicit an OT release in rat. It is unknown whether NK3R contributes to this endocrine response. Freely behaving male rats were administered an intraventricular pretreatment of 250 or 500 pmol of SB-222200, a specific NK3R antagonist, or 0.15 M NaCl before an intraperitoneal or intravenous injection of CCK-8 (nonsulfated or sulfated) or 0.15 M NaCl. Blood samples were taken before intraventricular treatment and 15 min after intraperitoneal or intravenous injection, and plasma samples were assayed for OT and VP concentration. Intraperitoneal injection of both nonsulfated and sulfated CCK-8 significantly increased plasma OT levels and had no effect on plasma VP levels. Intravenous injection of sulfated CCK-8 stimulated an increase in plasma OT levels and did not alter plasma VP levels. However, intravenous injection of nonsulfated CCK-8 stimulated a significant increase in plasma levels of both OT and VP. No other studies have demonstrated CCK-8-stimulated release of VP in rat. NK3R antagonist did not alter baseline levels of either hormone. However, pretreatment of NK3R antagonist significantly blocked the CCK-stimulated release of OT in all CCK treatment groups and blocked VP release in response to intravenous injection of nonsulfated CCK-8. Therefore, central NK3R signaling is required for OT and VP release in response to CCK administration.

vasopressin; oxytocin



Address for reprint requests and other correspondence: F. W. Flynn, Neuroscience Program, and Zoology and Physiology Dept., Univ. of Wyoming, Dept. 3166, Laramie, WY 82071 (e-mail: flynn{at}uwyo.edu)




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Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
G. E. Haley and F. W. Flynn
Blockade of NK3R signaling in the PVN decreases vasopressin and oxytocin release and c-Fos expression in the magnocellular neurons in response to hypotension
Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2008; 295(4): R1158 - R1167.
[Abstract] [Full Text] [PDF]




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