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July 1951


Author Affiliations


From the Research Division and the Frank E. Bunts Educational Institute, Cleveland Clinic Foundation.

AMA Arch Intern Med. 1951;88(1):1-8. doi:10.1001/archinte.1951.03810070011001

CONCEPTS of the pathogenesis of essential hypertension have fluctuated widely during the half-century in which this disease has been recognized. One view is that hypertension is of diverse, probably multiple, causation, dependent on factors broadly classified as neurogenic, cardiovascular, endocrine and renal.1 Among these, the participation of the nervous system was long ago considered especially significant, although no adequate explanation of the mechanism by which it might have this effect has been offered. Two observations in our experience pointed directly toward central nervous system participation in this disease. There were, first, the definition of the hypertensive diencephalic syndrome2 and, second, the demonstration of a pressor substance in the cerebral ventricular fluid of patients with hypertensive disease.3 Further, "neurogenic" hypertension has been defined as a common and early phase of essential hypertension.4

From the experimental aspect, Koch and Mies5 described, and others have confirmed, the production

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