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To the Editor:—
The concept of the pathogenesis of hypertension editorially reviewed in The Journal, May 10, 1948, however attractive from a clinical aspect, rests, unfortunately, on a tenuous chain of demonstrations. Among the experiments on which Heinbecker's new and elaborate concept is based, two facts seem to have been confirmed and to withstand critical appraisal: (1) neurohypophysial deficiency resulting from total or partial denervation of the gland and (2) nephrotoxic and vascular lesions due to desoxycorticosterone. On the other hand, seven bases for the concept have not yet had adequate experimental support: (1) that posthypophysial deficiency stimulates the eosinophils of the pars distalis, (2) that specific cardiotrophic and nephrotrophic effects may be ascribed to the eosinophils, (3) that adrenocorticotropin induces the secretion of desoxycorticosterone-like compunds, (4) that deficiency of the posthypophysis sensitizes to pressor agents, (5) that desoxycorticosterone causes a constriction of the efferent glomerular arterioles, (6) that the
Masson G. HYPERTENSION. JAMA. 1948;138(1):90. doi:10.1001/jama.1948.02900010092027
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