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Lowering of Blood Pressure and Modification of Hyperreactor Response in Hypertensive Patients

PAUL KEZDI, M.D.; ROBERT R. J. HILKER, M.D.

AMA Arch Intern Med. 1955;95(5):720-726.

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

Research in hypertension has been centered on the role of humoral influences and of increased sympathetic vasomotor tone. The increased sympathetic outflow in hypertension is attributed by some investigators to an abnormality in the hypothalamic circulatory centers or to a hyperirritable vasomotor center which responds to various stimuli by excessive vasoconstrictor impulses.* It seems unusual that research on the role of the sinoaortic regulatory mechanism has not advanced at a similar pace. Why this sensitive mechanism fails to control hypertension has not been thoroughly investigated. The questions of whether an increased sympathetic vasomotor tone is the result of a disturbed inhibitory function rather than primarily central in origin and whether this mechanism can somehow be altered in the hypertensive patient to again reduce the blood pressure to normal levels and to modify the hyperreactor response is completely unanswered. It is our intention to attempt to answer this question.

Certain fundamental . . . [Full Text PDF of this Article]

Author Affiliations
Chicago

From the Cardiovascular Laboratory, Department of Medicine, Chicago Wesley Memorial Hospital and Northwestern University Medical School.

Footnotes
Aided in part by a grant from the Lizzie K. Schermerhorn Memorial fund.

Preliminary report read before the Third Annual Convention of the American College of Cardiology, Chicago, May 27, 1954.