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NMDA Receptors in the Median Preoptic Area Mediate Hemodynamic Response Variability Following Stress
Author(s) -
Schwartz Julie Ann,
Reilly Nichole S,
Knuepfer Mark M
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a238-a
Subject(s) - median preoptic nucleus , nmda receptor , endocrinology , medicine , angiotensin ii receptor type 1 , angiotensin ii , receptor , circumventricular organs , dizocilpine , hypothalamus , preoptic area , subfornical organ
Stress produces a pressor response by eliciting an increase in sympathetic nerve activity. Central pathways that modulate sympathetic nerve activity include an angiotensinergic pathway that projects through the hypothalamus from circumventricular organs (CVOs) that bind peripheral angiotensin (AT) II. We have shown previously that blockade of AT 1 receptors in the hypothalamic median preoptic nucleus (mnPO) attenuates post‐stress increases in arterial pressure (AP). Additional evidence suggests that N ‐methyl‐d‐aspartate (NMDA) receptors are reported to be involved in the angiotensinergic signaling pathway in the mnPO. We investigated whether NMDA receptors in the mnPO were responsible for variable hemodynamic response patterns to stress. Cocaine evoked a pressor response in Sprague‐Dawley rats due, in some rats (vascular responders or VR), to a large increase in systemic vascular resistance (SVR) and, in other rats (mixed responders or MR), to smaller increases in SVR and an increase in cardiac output (CO). Administration of an NMDA receptor antagonist, dizocilpine (MK801, 20 nmol in 100 nl), prevented the large increase in SVR and the decrease in CO in VR in response to cocaine without altering the responses in MR. These results demonstrate that signaling through the mnPO produces different response profiles to stress in MR and VR rats. We conclude that NMDA and AT 1 receptors mediate the greater increase in SVR in VR compared to MR. This work was supported by USPHS DA13256, GM008306, and a grant from the American Heart Association, Heartland Affiliate.