Repeated attempts to produce hypertension (HT) through psychological stress hare failed to elevate blood pressure (BP) to levels seen in chronic, untreated essential HT in humans. In general, these studies have two characteristics in common: they utilize the nonnotenslve animal, with no genetic history of HT, and they involve stressors to which animals readily adapt. The present study utilized offspring with one HT parent. The male F, offspring of SHR X WKY had borderline HT (X ± SEM = 152.4 ± 134 mm Hg). With a conflict paradigm used as the stressor, experimental animals eventually developed severe HT (188.3 ± 2.70 mm Hg) compared to two non-stressed control groups (158.4 ± 2.31 mm Hg and 151.9 ± 2.25 mm Hg). After 15 weeks of stress for 2 hours daily, termination of conflict for 10 weeks did not reduce the HT in experimental animals. Subsequent analyses revealed that stressed animals, when compared to nonstressed controls, exhibited elevated heart-weight-to-bodyweight ratios and significant cardiac pathology in the form of myofibrillar degeneration, accumulation of inflammatory cells, and flbrosis. The implications of using this model for the analysis of cardiovascular concomitants of stress-induced HT are discussed. (Hypertension 3: 496-505, 1981) KEY WORDS • stress-induced hypertension systolic blood pressure cardiac pathology • borderline hypertensive rat
Studies of aversive conditioning in animals have seldom elicited tonic elevations in blood pressure (BP) equivalent to those which produce pathological changes in humans. While it is possible that psychological factors are not that important in the etiology of hypertension, it is also possible that the failure to elicit large tonic elevations in BP in animals may be due either to stressors which are insufficiently potent and/or to an inadequate physiological model. The present study sought to maximize the probability of producing large tonic changes in BPs by using a conflict paradignt in a genetic strain of rats which develops systolic BPs in the borderline hypertensive area (c. 150 mmHg). Forty‐eight male F1 generation offspring of spontaneously hypertensive rats mated with normotensive controls were randomly split into three groups: experimental (subjected to 3 weeks of avoidance training and 12 weeks of conflict in conditioning cages), mild restraint control (placed in conditioning cages daily but not shocked), and maturation control (neither shocked nor restrained) groups. Animals subjected to conflict gradually developed tonic levels of systolic BP well into the hypertensive range (c. 185 mmHg). Restraint control animals also showed some elevation (c. 165 mmHg), but maturational controls showed no change (c. 150 mmHg). The saliency of this animal model for the study of stress‐induced hypertension is discussed.
1. This study sought to develop an animal model which would be prone to stress-induced hypertension without spontaneously developing it. 2. Eighteen male rats, F1 offspring of spontaneously hypertensive x Wistar-Kyoto rats, had tail-cuff systolic blood pressures of 152 mmHg at 12 weeks of age. Animals were randomly assigned to three groups of six each: experimental (subjected to 'conflict' 2 h daily for 12 weeks), restraint control (placed in conditioning cages but not subjected to conflict) and maturation control (neither restrained nor stressed). 3. Systolic blood pressure rose significantly in experimental animals to 186 mmHg. Experimental animals studied for a 10 week follow-up period without conflict maintained the elevated pressure. In addition, these animals showed myofibrillar degeneration and an elevation in heart weight/body weight ratios. Restraint animals showed a modest elevation in pressure during the study, but not during the 10 week follow-up. Maturation animals showed no changes in blood pressure. 4. The development of a model of hypertension combining genetics with psychological stress may serve as a means for determining the factors involved in triggering and sustaining stress-induced hypertension which may prove relevant to essential hypertension in man.
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