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This Article Full Text Full Text (PDF) All Versions of this Article: 90/1/141    most recent expphysiol.2004.028308v1 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 McDougall, S. J. Articles by Widdop, R. E. Search for Related Content PubMed PubMed Citation Articles by McDougall, S. J. Articles by Widdop, R. E. Related Collections Autonomic Neuroscience

¹ Department of Pharmacology, Monash University, Victoria 3800, Australia

The aim of this study was to determine to what extent stress-induced cardiovascular responses depend upon rat strain and/or stressor. Spontaneously hypertensive rats (SHRs), Wistar-Kyoto rats (WKYs) and Sprague-Dawley (SD) rats were implanted with telemetry probes in order to measure heart rate and blood pressure changes when exposed to a stressor. The stress protocols employed included handling, air-jet and restraint, where each stressor was repeated over 10 consecutive days. In addition, a heterologous protocol was established whereby the experimental groups having experienced 10 days of air-jet stress were then immediately exposed to 10 consecutive days of restraint. Each stressor caused graded tachycardic and pressor responses in all strains. For all strains, the magnitude and duration of heart rate and blood pressure increases were greatest in the restraint-based protocols while handling and air-jet caused submaximal changes. A comparison between strains indicated that SHRs exhibited prolonged pressor responses to each of the stressor types tested as compared to the normotensive strains. In addition, repeated exposure over 10 days to handling and air-jet in SHRs caused tachycardic and/or pressor responses to adapt to ‘normotensive-like’ levels. Heterologous restraint stress caused sensitization of cardiovascular responses upon first exposure, predominantly in normotensive strains. Collectively these data show that the magnitude and duration of the tachycardia and pressor responses evoked by the stressors were different within the strains and were also modified by prior experience. In addition, the cardiovascular profiles presented in this study demonstrate that, within each strain, the heart rate response during stress is graded according to the type of stressor encountered.

(Received 13 June 2004; accepted after revision 20 October 2004; first published online 12 November 2004)
Corresponding author R. E. Widdop: Department of Pharmacology, Monash University, Victoria 3800, Australia. Email: robert.widdop{at}med.monash.edu.au

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