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Role of sympathetic blockade in the therapy of hypertension

Authors
Journal
The American Journal of Medicine
0002-9343
Publisher
Elsevier
Publication Date
Volume
8
Issue
3
Identifiers
DOI: 10.1016/0002-9343(50)90067-2
Disciplines
  • Biology
  • Chemistry
  • Medicine
  • Pharmacology

Abstract

Abstract The role of adrenergic blockade in the therapy of hypertension is still obscure. Pharmacologic advances during the last few years have led to the development of agents capable of producing a clinically useful “chemical sympathectomy.” Such agents are very effective in lowering the blood pressure in cases of neurogenic (sympatho-adrenal) hypertension. At the present time pheochromocytoma and intracranial lesions are the only causes of human hypertension which are definitely known to involve overactivity of the sympatho-adrenal system. However, presumptive evidence is accumulating to indicate that neurogenic factors may be involved in early essential hypertension and it is possible that adequate adrenergic blockade early in the course of such hypertension may be effective in aborting its development. Only additional evidence regarding the etiology of essential hypertension and further clinical trial of adrenergic blockade can define the extent to which this possibility may be realized. Of the compounds currently employed for the production of adrenergic blockade, the β-haloalkylamines appear to be the most promising. They are the most specific, effective and persistent of the available agents. The dihydro ergot alkaloids are much more effective than their non-hydro-genated congeners. However, at present much of the experimental work on these compounds is complicated by the marked depressant effects which they exert upon vasomotor reflexes and the vasomotor center and by their stimulant action on the vagal nuclei. The clinical administration of the dihydro compounds has been seriously limited by their very potent emetic action. Significant specific adrenergic blockade has not yet been produced in humans by members of the ergot series. A third group of adrenergic blocking agents to receive recent attention, the imidazolines, appear to cause so much cardiac stimulation that no consistent lowering of the blood pressure is observed when they are administered to either animals or man. It should be emphasized that research in the field of adrenergic blockade need not be limited to members of series now known to be active. The three groups of the aforementioned compounds are structurally unrelated; only four years ago the β-halo-alkylamines were completely unknown as adrenergic blocking agents. The cooperation of synthetic chemists and pharmacologists in the study of series of compounds unrelated chemically to those listed here may provide the solution in the search for an agent producing a fully satisfactory “chemical sympathectomy.”

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