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DOI‐evoked pressor and tachycardia from the anterior hypothalamic/preoptic area (AH/PO) is mediated by sympathoexcitation, vasopressin and angiotensin
Author(s) -
Martin John R.
Publication year - 2007
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.21.6.a879-c
Subject(s) - ritanserin , endocrinology , medicine , vasopressin , yohimbine , vasopressin receptor , agonist , microinjection , receptor antagonist , prazosin , angiotensin ii , blood pressure , antagonist , receptor
Microinjection of the serotonin (5‐HT) 2A/2C receptor agonist DOI into the AH/PO of rats evokes pressor and tachycardic responses. The present study was done to determine the mechanism by which DOI evokes these changes. Male Sprague‐Dawley rats were anesthetized, and catheters placed into the right femoral artery and vein for monitoring blood pressure (BP) and for drug administration, respectively. A guide cannula was targeted to the left AH/PO for DOI microinjection. The systemic presence of pentolinium (PENT), d[(CH 2 ) 5 Tyr(Me)]AVP (AVPX), the combination of prazosin (PRAZ) and yohimbine (YOH), or the combination of PRAZ, YOH and AVPX did not affect, whereas the combination of PENT and AVPX attenuated, the increase in BP evoked by DOI. In all cases the presence of PENT prevented the tachycardia. Adding ZD 7155 (an AT 1 receptor antagonist) to PENT and AVPX, or the prior administration of ritanserin (a 5‐HT 2 receptor antagonist) into the AH/PO prior to DOI completely blocked the DOI‐evoked responses. These results suggest that the cardiovascular responses evoked by DOI administration into the AH/PO involve the 5‐HT 2 receptor, sympathoexcitation, vasopressin and angiotensin. Supported by NHBLI 77194.