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, [00BB]Pitressin[00AB] and nephrectomy, in an attempt to produce cardiopathy; Crane et al. (1958 b) employed laparotomy, skin excision, hemorrhage, burns, fractures, limb ligation and formaldehyde injections, in an effort to produce hypertensive cardiovascular disease. Virtually all of the Stressors cited are known to produce shock. Their failure to produce hypertensive cardiovascular disease is there¬ fore perhaps not surprising. Although most Stressors share the ability to activate the pituitary-adrenal axis, the action of the adrenal hormones thus evoked upon the cardiovascular system is strongly conditioned, either positively or nega¬ tively, by a variety of circumstances. It seems unreasonable to expect a Stressor capable of inducing a hypotensive shock-like state, to produce hypertensive cardiovascular disease.Although it is often assumed -incorrectly -that Selye's theory requires that the property should be shared by a wide variety of Stressors having the capacity