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Vasopressin V₁ receptors contribute to hemodynamic and sympathoinhibitory responses evoked by stimulation of adenosine A_2a receptors in NTS

Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan

Submitted 29 September 2005 ; accepted in final form 6 December 2005

Activation of adenosine A_2a receptors in the nucleus of the solitary tract (NTS) decreases mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), whereas increases in preganglionic adrenal sympathetic nerve activity (pre-ASNA) occur, a pattern similar to that observed during hypotensive hemorrhage. Central vasopressin V₁ receptors may contribute to posthemorrhagic hypotension and bradycardia. Both V₁ and A_2a receptors are densely expressed in the NTS, and both of these receptors are involved in cardiovascular control; thus they may interact. The responses elicited by NTS A_2a receptors are mediated mostly via nonglutamatergic mechanisms, possibly via release of vasopressin. Therefore, we investigated whether blockade of NTS V₁ receptors alters the autonomic response patterns evoked by stimulation of NTS A_2a receptors (CGS-21680, 20 pmol/50 nl) in -chloralose-urethane anesthetized male Sprague-Dawley rats. In addition, we compared the regional sympathetic responses to microinjections of vasopressin (0.1–100 ng/50 nl) into the NTS. Blockade of V₁ receptors reversed the normal decreases in MAP into increases (–95.6 ± 28.3 vs. 51.4 ± 15.7 %), virtually abolished the decreases in HR (–258.3 ± 54.0 vs. 18.9 ± 57.8 beats/min) and RSNA (–239.3 ± 47.4 vs. 15.9 ± 36.1 %), and did not affect the increases in pre-ASNA (279.7 ± 48.3 vs. 233.1 ± 54.1 %) evoked by A_2a receptor stimulation. The responses partially returned toward normal values 90 min after the blockade. Microinjections of vasopressin into the NTS evoked dose-dependent decreases in HR and RSNA and variable MAP and pre-ASNA responses with a tendency toward increases. We conclude that the decreases in MAP, HR, and RSNA in response to NTS A_2a receptor stimulation may be mediated via release of vasopressin from neural terminals in the NTS. The differential effects of NTS V₁ and A_2a receptors on RSNA versus pre-ASNA support the hypothesis that these receptor subtypes are differentially located/expressed on NTS neurons/neural terminals controlling different sympathetic outputs.

nucleus tractus solitarii; purinoceptors; vasopressin V₁ receptor antagonist; adrenal sympathetic nerve; renal sympathetic nerve

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