Very high levels of circulating catecholamines, as seen in pheochromocytoma, will cause hypertension. But, less is known about more subtle functions within the central nervous system that can produce or prevent chronic hypertension. Attempts to develop a suitable animal model of neurogenic model remain controversial. Baroreceptor denervation was thought to produce hypertension by way of unchecked increases in sympathetic outflow. However, protocols utilizing continuous monitoring of blood pressure have indicated that lability, rather than the mean value of pressure, is increased in many instances. Lesions placed in the central nervous system have usually produced either a short-term fulminating hypertension or increased pressure lability only, but ablation of the nucleus of the tractus solitaris has now been shown to produce sustained increases in blood pressure. Recent studies have also indicated that there are permissive neural factors; normal nervous function is needed for the production of several types of experimental hypertension. In some instances, chronic hypertension has been produced using imposed stresses that presumably increase sympathetic activity.
KeywordsChronic Hypertension Tractus Solitaris Renal Denervation Suitable Animal Model Experimental Hypertension
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