Spontaneous remission of hypertension in awake rats chronically exposed to shaker stress.

Abstract

SUMMARY Hypertension was induced experimentally by subjecting rats to vigorous shaking, 4 hours (at random) daily for 14 weeks. Systolic pressures measured with the tail-cuff method began to rise after the first week and were significantly derated on Weeks 3, 4, 6, 7, and 8, but reverted to normotensive levels thereafter despite continued shaking. A similar hypertension was then induced in another group of rats and when spontaneous remission occurred, pressor responsiveness was tested on the eleventh week by recording aortic pressures from indwelling catheters. Pressor responses to further shaking or electrical stimulation of the anterior hypothalamus were smaller in shaker-stressed than in control rats, while those to injected norepinephrlne were almost the same in both groups. Spike potentials recorded from postganglionlc sympathetic (splanchnic) nerves showed higher baselines but smaller increases in neural firing during hypothalamic stimulation in shaker-stressed than in control rats. These results suggest that while shaker stress alone can induce hypertension, the resulting blood pressure elevation is not sustained, perhaps because adaptation within the central nervous system concurrently reduces pressor responsiveness. action to stress, and based on the assumption that with frequent repetition the pressure elevation eventually becomes sustained, chronic exposure to stress has often been used for inducing experimental hypertension. Air blasts, 1 intermittent decompression, 2 aversive operant conditioning,' psychosocial stimuli, 4 and a mixture of shaking, noise, and flashing lights," have all been found effective in making rats hypertensive. Because the hypertension thus induced can be prevented by chemical sympathectomy with 6-hydroxydopaminc" or by doses of amethyl tyrosine that deplete brain catecholamines selectively, 7 the involvement of central sympathetic mechanisms has been proposed. Chronic exposure to noise and flashing lights requires a precisely controlled laboratory environment that is more elaborate and expensive to set up than one based on shaking alone. Whether shaking (henceforth referred to as shaker 311 stress), which is more potent than either noise or flashing light in eliciting pressor or tachycardiac effects," can induce hypertension when applied alone is unknown. While attempting to resolve this question, we found the resulting blood pressure elevation unsustained. Consequently, additional experiments were done to determine whether pressor and neural responses to hypothalamic stimulation had been altered by previous exposure to shaker stress.Methods Two groups of 7-week-old female rats of the Sprague-Dawley strain, were purchased from Hilltop Laboratory Animals, Inc. (Chatsworth, CA) and randomly divided into control and experimental subgroups. Of 18 rats in the first group, half were used as controls and the others exposed to shaker stress manipulation for 14 weeks while systolic pressures, heart rates, and body weights were measured once weekly. A second group of 24 rats (12 contro...

Effects of taurine on stress-evoked hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats.

“…26 Our preliminary experiments indicated that, compared with a stimulus such as noise or flashing, shaker stress produced circulatory reactions varying much less in degree and duration from rat to rat during a certain period. We applied an acute, single stress to prevent the problems of habituation, which appear to differ in a complex way between the SHR and WKY.…”

“…25 We postulated that taurine might attenuate stressevoked alterations in hemodynamics and sympathoadrenal activity in the hyperreactive SHR. In the present study, we assessed cardiovascular hemodynamics and sympathoadrenal activity at rest and during shortterm shaker stress 26 in conscious SHR and normotensive Wistar-Kyoto rats (WKY) with or without longterm taurine pretreatment.…”

Cardiovascular responses to acute stress in young-to-old spontaneously hypertensive rats.

“…36 The proposed mechanisms of such stress hyperreactivity in SHR include genetically determined central hyperresponsiveness, 1 ' 18 " 20 '" reduced sensitivity of baroreceptor reflexes, 3 * and peripheral factors such as increased vascular smooth muscle sensitivity and structural hypertrophy. '• w In view of the nature of shaker stress 31 and the response patterns of blood flow and catecholamines, alterations in the central nervous system, presumably the limbic and hypothalamic areas participating in the defense reaction, are deemed to be most important.…”

Animal models for the study of primary and secondary hypertension in humans

“…Environmental stress, including separate or simultaneous introduction of flashing lights, loud noises and oscillating cages (55–57), or long-term exposure to high salt, fat or sugar in the diet, can be used to induce hypertension (58). Extremes of temperature, particularly coldness, also induces a hypertensive phenotype, as observed in rats exposed to 5°C for 3 weeks (59).…”