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Repeated attempts to produce hypertension (HT) through psychological stress have 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 normotensive 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 F1, offspring of SHR x WKY had borderline HT (-/x +/- SEM = 152.4 +/- 1.34 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-body-weight ratios and significant cardiac pathology in the form of myofibrillar degeneration, accumulation of inflammatory cells, and fibrosis. The implications of using this model for the analysis of cardiovascular concomitants of stress-induced HT are discussed.
Lawler et al. (Wed,) studied this question.