The central nervous system may initiate or maintain hypertension in humans by a variety of mechanisms. Increased cerebral pressor activity can cause hypertension in some patients with the Guillain-Barré syndrome, where disinhibition of cerebral centres may result from an afferent baroreflex lesion. The brain itself initiates hypertension in patients with cerebral tumours, cerebrovascular accidents, and subarachnoid haemorrhage. The use of drugs (including alcohol), or at times their withdrawal, results in hypertension through neurogenic mechanisms. Impaired cerebral activity also contributes, as in tetraplegic patients in whom paroxysmal hypertension is a consequence of increased spinal sympathetic reflex activity, which is not restrained or appropriately counteracted by the brain because of the cervical spinal cord transection. Neurogenic factors also play a role in the maintenance of hypertension in patients in whom the initiating cause is clearly humoral. In renal artery stenosis for instance, cerebral actions of angiotensin II may later gain ascendance over its peripheral effects, especially as circulating levels fall, as has been demonstrated with the centrally acting sympatholytic agent, clonidine. This is an example of humoroneural coupling that contributes to the hypertension. Increased afferent renal nerve activity may be an additional factor, especially in patients with renal parenchymal disease, where renin appears to play a minor role. The role of the nervous system in other causes of primary hypertension is presently less clear. In phaeochromocytoma noncatecholamine tumour products may have neurogenic effects that could account for the ability of clonidine to lower blood pressure in some patients. These are examples by which the central nervous system plays a role in either initiating, or more importantly, in perpetuating hypertension, even when the primary cause is clearly nonneurogenic. The refinement of existing techniques and development of noninvasive approaches, together with the study of patients with welldefined neurological disorders, should further extend our knowledge of the role of the central nervous system in circulatory control, especially in the pathophysiology of essential and secondary hypertension. Determination of the neural mechanisms is likely to influence patient management and future therapeutic strategies.
Address correspondence and reprint requests to Dr. C. J. Mathias at Medical Unit, St. Mary's Hospital and Medical School, Norfolk Place, London, W2 1PG England.
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