(Hypertension. 2000;35:126.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
From the Department of Pharmacology, Monash University, Clayton, Victoria, Australia.
Correspondence to Dr Andrew J. Lawrence, Department of Pharmacology, Monash University, Wellington Road, Clayton, Victoria 3168, Australia. E-mail andrew.lawrence{at}med.monash.edu.au
AbstractWith the use of a restraint stress paradigm, both normotensive Wistar-Kyoto (WKY ) rats and spontaneously hypertensive rats (SHR) underwent acute (1-hour restraint in a Perspex tube), chronic (1-hour restraint for 10 consecutive days), or no-restraint (control) stress. Rats experiencing chronic restraint were previously implanted with telemetric probes to measure heart rate and blood pressure. Basal (prestress session) cardiovascular variables did not change during the course of the study (SHR: mean arterial pressure 129±1 mm Hg, heart rate 288±4 bpm; WKY rats: mean arterial pressure 103±1 mm Hg, heart rate 285±3 bpm). Restraint caused tachycardia and pressor responses in the WKY rats and SHR, but these effects were greater in the hypertensive strain. The duration of restraint-induced tachycardia did not change in the WKY rats between acute and chronic stress; however, a graded reduction in the duration of restraint-induced tachycardia occurred in the SHR, decreasing to WKY rat levels by day 7 of the 10-day regimen. These data indicate that although the WKY rats can effectively "cope" within a single period of restraint, the coping mechanism is apparently impaired in the SHR compared with the WKY rats. A reduced capacity to cope with processive stressors may thus have an affect on cardiovascular regulation and represent an additional risk factor in hypertension.
Key Words: stress hypertension tachycardia
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