Many attempts have been made to demonstrate that stressed uninephrectomized rats on a high NaCl intake develop hypertensive cardiovascular disease. This was first claimed by Selye (1943), who inferred that adrenal cortical hypersecretion was the causative factor. Recently the experimental data has been reinforced and the view as to causation reiterated (Selye, 1957, Ingle & Baker, 1957, and others). Crane et al. (1958 a) have subjected the hypothesis to careful scrutiny and concluded that while exposure to cold, or certain other stressors, produces cardiac and renal hypertrophy and a variable incidence of pathologic changes in these organs, the amount of food consumed, and particularly sodium ingested, are crucial factors. A bewildering variety of stressors has been tried. Selye et al. (1958) used restraint, pentobarbital, vagotomy, cold baths, hot baths, spinal cord transection, bone fractures, intestinal trauma, quadriplegia, adrenalin, noradrenalin, »Pitressin« and nephrectomy, in an attempt to produce cardiopathy; Crane et