Abstract
The administration of DOCA to unilaterally nephrectomized rats given a high NaCl intake caused an intense saline polydipsia and induced hypertensive vascular disease accompanied by cardiac hypertrophy in Sprague—Dawley animals. Similarly treated Long—Evans rats developed none of these changes, although they readily developed them when subjected to enucleation of the adrenal glands. These findings would seem to be incompatible with the assumption that adrenal—regeneration hypertension (ARH) is due to endogenous DOC hypersecretion by enucleate adrenal glands. The possibility is moot: evidence both for and against such an altered steroid secretory pattern has been presented from other laboratories. If so, it may well contribute to the response, but in view of the observation that Long—Evans rats are highly refractory to the development of DOCA hypertension but highly susceptible to ARH, it can hardly be held solely responsible. (Endocrinology 92: 1175, 1973)
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