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1 Graduate Neuroscience Program, University of Wyoming, Laramie, Wyoming, United States
2 Zoology and Physiology Department, University of Wyoming, Laramie, Wyoming, United States; Graduate Neuroscience Program, University of Wyoming, Laramie, Wyoming, United States
* To whom correspondence should be addressed. E-mail: flynn{at}uwyo.edu.
Activation of the neurokinin 3 receptor (NK3R) by a receptor agonist, hypotension, and hyperosmolarity results in the internalization of NK3R expressed by magnocellular neurons and the release of vasopressin (VP) and oxytocin (OT) into the circulation. The contribution of NK3R activation to the release of VP and OT in response to hyperosmolarity and hypotension was evaluated by measuring the release of both hormones following pretreatment with a selective NK3R antagonist, SB-222200. Freely behaving male rats were given an intraventricular injection of either 0.15 M NaCl, 250 pmol, 500 pmol, or 1000 pmol SB-222200, and then administered an intravenous infusion of 2 M NaCl or 0.15 M NaCl (Experiment 1), or a bolus intravenous injection of 0.15 M NaCl or hydralazine (HDZ), a hypotension-inducing drug (Experiment 2). Blood samples were taken from indwelling arterial catheters at various time points for 1-2 hours, both before and after treatments. Plasma VP and OT levels were determined by ELISA. Blockade of NK3R did not affect the baseline levels of either hormone. In contrast, pretreatment with SB-222200 significantly reduced (~60%) or abolished the release of VP and OT, respectively, to 2 M NaCl infusion. HDZ-induced VP and OT release was eliminated by pretreatment with 500 pmol SB-222200. Therefore, NK3R activation contributes significantly to the systemic release of both VP and OT in response to osmotic and hypotensive challenges.
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