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ROBERT D. TAYLOR, M.D.; IRVINE H. PAGE, M.D.; A. C. CORCORAN, M.D.

AMA Arch Intern Med. 1951;88(1):1-8.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
CLEVELAND

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

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