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This Article Full Text Full Text (PDF) All Versions of this Article: 297/2/R495    most recent 00232.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Vianna, D. M. L. Articles by Carrive, P. PubMed PubMed Citation Articles by Vianna, D. M. L. Articles by Carrive, P.

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Inhibition of the cardiovascular response to stress by systemic 5-HT_1A activation: sympathoinhibition or anxiolysis?

School of Medical Sciences, University of New South Wales, New South Wales, Australia

Submitted 27 April 2009 ; accepted in final form 9 June 2009

5-HT_1A agonists given systemically are known to produce anxiolytic effects. In addition, a growing body of research is showing that those compounds also have central sympathoinhibitory properties. Since emotional arousal gives rise to sympathetic activation, it is not clear whether systemic treatment with a 5-HT_1A agonist reduces the sympathetic response to emotional stress primarily by a direct action on sympathetic-related sites in the brain or indirectly through reducing anxiety. To test this, we compared the effect of intraperitoneal injections of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.05 and 0.25 mg/kg), a preferential 5-HT_1A agonist, or vehicle on the cardiovascular responses to four stressors known to produce sympathetic activation, three being emotional stressors, and one physiological. In conscious rats, 30-min exposure to either a neutral context, a fear-conditioned context, or to restraint stress led to increases in heart rate and blood pressure, which were attenuated by 8-OH-DPAT. In contrast, the same treatment did not reduce the cardiovascular response to 30-min cold exposure (4°C). The results suggest that 8-OH-DPAT acts preferentially on limbic, rather than central, autonomic sites. Hence, doses of 5-HT_1A agonists, which are just sufficient to produce anxiolysis, are not enough to cause true sympathoinhibition.

sympathetic responses; freezing; anxiety; cold defense; tachycardia