Abstract

Dr. Conway reviewed his test for differentiating hypertensive patients into those with and without altered vascular elasticity. The discussion then turned to the role of the nervous system in hypertension. Experiments concerning the role of neural influences in initiating permanent hypertension were reviewed by Drs. McCubbin, Wakerlin, Langford, and Stamler. The Dock experiment of pithing hypertensive animals was then considered. His results seemed to indicate the importance of neural influences in maintaining experimental renal hypertension, but it was agreed that it was not justifiable to conclude from this work that renal hypertension was maintained by elevated neural tone (Drs. Braun-Menéndez, Bohr, Goldblatt, Kezdi, and Sapirstein). The conferees then examined the question of increased neurogenic arteriolar tone in human essential hypertension. The lack of evidence for increased neural tone, based on the failure of greater dilation following ganglionic blockade in the hypertensive subject was supported by Dr. Hoobler and opposed by Dr. Kirkendall. Most agreed that inferences from changes in peripheral resistance after blockade were fraught with error, due to the intrinsic elasticity of the arterioles (Dr. Beck), the predominance of venomotor blockade (Dr. McCubbin), the "break through" of buffer reflexes (Drs. McCubbin, Kezdi, Stamler), and the effects of varying types of anesthesia in animal experiments (Dr. Stamler). Finally, in reply to a question concerning ways to produce chronic, sustained, experimental, neurogenic hypertension, Dr. McCubbin mentioned the experiments of Taylor and Page, and Dr. Wakerlin concluded with a description of a technic for producing in dogs chronic neurogenic hypertension which had persisted in excess of 4 years. This consisted in applying a constricting plastic clamp to the carotid sinus area bilaterally, so as to reduce the volume pulse of the arterial branches of the sinus by two-thirds.

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