Baroreflex function in chronically stressed borderline hypertensive rats

• Published in: Physiology & behavior Vol. 49; no. 3; p. 539
• Main Authors: Lawler, J E, Sanders, B J, Cox, R H, O'Connor, E F
• Format: Journal Article
• Language: English
• Published: United States 01.03.1991
• Subjects: Angiotensin II - pharmacology; Animals; Arousal - drug effects; Arousal - physiology; Blood Pressure - drug effects; Blood Pressure - physiology; Electroshock; Female; Hypertension - physiopathology; Male; Pressoreceptors - drug effects; Pressoreceptors - physiopathology; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Reflex - drug effects; Reflex - physiology; Stress, Psychological - complications; Stress, Psychological - physiopathology
• ISSN: 0031-9384
• DOI: 10.1016/0031-9384(91)90277-U

A number of previous studies have demonstrated that some aspect of baroreflex function is altered as hypertension develops. However, no studies have determined whether a chronic stressor can alter baroreflex function in the resting state. In the present study, male borderline hypertensive rats (BHR) were divided into three groups: control, stressed daily for 5 weeks, and stressed daily for 11 weeks. At the appropriate time, 7 different dosages of angiotensin II (AII) were given intravenously as a bolus injection. Heart rate (interbeat interval, or IBI) and mean arterial pressure were tracked for 90 subsequent beats. For each group, intercorrelations between pressure and IBI were obtained. In addition, overall means of pressure and IBI for each dosage were computed for each group and plotted. Higher dosages of AII were required to produce a significant correlation between pressure and IBI in the 5-week group compared to control. In the 11-week group, only the highest dosage yielded a significant correlation between pressure and IBI. When data were expressed in terms of the highest pressure and its corresponding IBI for each group, the 5-week-stress group had a shift in set point compared to control. The 11-week group showed a shift in set point and a reduction in gain compared to control animals. The similarity between these findings and those for other models of hypertension is discussed, with special emphasis on the potential role of the central nervous system.