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This Article Full Text Full Text (PDF) All Versions of this Article: 89/5/549    most recent expphysiol.2004.027714v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bernatova, I. Articles by Morris, M. Search for Related Content PubMed PubMed Citation Articles by Bernatova, I. Articles by Morris, M. Related Collections Genomic Physiology

¹ Department of Pharmacology and Toxicology, Wright State University School of Medicine, Dayton, Ohio,² Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic and³ Department of Physiological Sciences, Fundacao Faculdade Federal de Ciencias Medicas, Porto Alegre, Brazil

We used oxytocin knockout (OTKO) mice to investigate the role of oxytocin in regulation of blood pressure, heart rate and stress reactivity (pressure reactivity and plasma corticosterone). Male OTKO and control wild-type mice with carotid arterial catheters were exposed to intermittent shaker stress for 7 days (2 min stressors, 45 times per day). Mean arterial pressure (MAP) and heart rate (HR) were recorded continuously (24 h) before stress (basal), on stress days 1, 3 and 7 (S1, S3 and S7) and 1 day poststress (recovery). Plasma corticosterone (Cort) was measured before stress and 30 min after the last stress on day 7. Twenty-four hour averages of MAP and HR were lower in OTKO mice than in controls (P < 0.0001 and P < 0.005, respectively) with a significant diurnal rhythm. Chronic stress (S1 and S3) produced an increase in 24 h average MAP in OTKO mice, but not in controls. There were no stress-related changes in 24 h average HR values between control and OTKO mice. The immediate pressor responses were analysed during the dark and light periods (19.00 and 08.00 h). During the dark period, stress-induced pressor responses were observed only in OTKO mice (S1 and S3). In the light period, stress-induced MAP increases were seen on all days in OTKO mice and on days S1 and S3 in controls. There were no differences in baseline Cort between the groups; however, OTKO mice showed a reduced response to chronic stress (+298 versus+411%, OTKO mice versus controls, P < 0.005). In conclusion, oxytocin deficiency alters the endocrine and pressor responses to chronic stress, suggesting that the endogenous oxytocin system is important in regulating the stress-induced pressor response.

(Received 25 March 2004; accepted after revision 27 May 2004; first published online 7 June 2004)
Corresponding author M. Morris: Department of Pharmacology and Toxicology, Wright State University School of Medicine, 3640 Colonel Glenn Highwayy, Dayton, OH 45435, USA. Email: mariana.morris{at}wright.edu

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