Neurogenic pressor episodes fail to cause hypertension, but do induce cardiac hypertrophy.

Abstract

Repeated neurogenic pressor episodes by hindquarter compression were elicited in nine experimental dogs. Conscious dogs underwent 6 hours of compression every day over a period of 9 weeks. The average mean blood pressure increase during the compression periods was 25 mm Hg, but after decompression the blood pressure promptly returned to baseline values. This blood pressure response was constant and did not change over the 9-week period. The blood pressure increase was associated with a significant increase of plasma norepinephrine values. After validity of the model was established, echocardiographic measurements were performed at baseline and after 3, 6, and 9 weeks of compression in six experimental and six time-control dogs. Concentric left ventricular hypertrophy was already detectable at 3 weeks, and at the ninth week, the left ventricular mass was 28% above the baseline value T wo notions are deeply engrained in the traditional thinking about hypertension. The first is that patients with hypertension undergo a phase of "labile" neurogenic hypertension 1 that eventually, through the cumulative effect of pressor episodes, leads to sustained hypertension.2 Second is that labile blood pressure per se is an innocuous condition 3 and that target organ damage is a relatively late complication of sustained hypertension. This attitude largely determines the rather cautious "wait until the blood pressure is permanently elevated" approach to antihypertensive treatment. 4 However, practicing physicians increasingly recognize that some patients with even the mildest forms of hypertension already show signs of left ventricular hypertrophy and that such patients may require early treatment. Received September 21, 1988, accepted December 5, 1988 We developed a model to elicit repeated pressor episodes in dogs. 56 The following lines of evidence obtained in chloralose-anesthetized animals indicate that the blood pressure increase during compression is neurogenic: 1) blood pressure elevation is associated with increase of plasma norepinephrine and plasma renin as well as an acceleration of heart rate; 2) the increase of blood pressure, plasma norepinephrine, and renin are abolished by a low spinal anesthesia; 3) hemodynamically the blood pressure increase is due to an elevation of vascular resistance, and both high resistance and blood pressure are abolished with ganglionic blockade; and 4) the blood pressure response is not altered when the circulation to the hindquarter has been severed through ligation of the vena cava and the lower aorta. This, in turn, suggests that the afferents for the reflex originate in the hindquarters and proves that the response is not dependent on distant effects of the translocated blood or chemical effluents from the compressed area. Our results have been confirmed by Bradley and Hjemdahl 7 who linked the blood pressure response to enhanced neurogenic drive to the kidneys.This model offers unique opportunities to study the effects of transient blood pressure elevation on by guest on May 11, ...

Metabolic syndrome in subjects with white-coat hypertension: impact on left ventricular structure and function

“…In this context, it has been demonstrated that periods of neurogenic pressor episodes without permanent hypertension can cause LV hypertrophy in dogs. 30 Therefore, it could be speculated that frequent BP peaks triggered by alerting reactions may contribute to the rise in long-term cardiovascular risk.…”

Sympathoadrenal Stress Reactivity Is a Predictor of Future Blood Pressure

“…34,40 One possible mechanism explaining the actual relationship between stress reactivity and development of hypertension could be the direct effect of frequent increases in blood pressure on the vasculature. However, transient blood pressure elevations are not capable of developing sustained blood pressure elevations, per se, in animal models, 11,12 although care should be taken to extrapolate these findings to humans. Our data indicate that activity in the sympathetic nervous system may have implications for later development of hypertension independent of blood pressure.…”

“…Intermittent pressure elevations could lead to structural vascular changes, but attempts to produce irreversible, sustained blood pressure elevations purely as a consequence of transient increases of blood pressure in dogs have not been successful. 11,12 Another possible link between hyperreactivity and development of hypertension is a direct effect of catecholamines. Sympathetic stimulation is known to be a trophic factor for vascular hypertrophy.…”

Prognostic significance of blood pressure measured on rising

“…For example, it has been shown in animals that transitory elevations in BP (6 h per day) can induce LV hypertrophy (LVH). 10 The elevation in BP on rising may last several hours, as BP tends to be higher in the morning. 11 We showed in a population of 181 untreated hypertensive patients that the value of BP on rising is as well correlated with LVM of hypertensives as the mean 24-h value.…”