Deficiency of Deoxycorticosterone-Binding Protein in the Hypothalamus of Rats Resistant to Deoxycorticosterone-Induced Hypertension1

Abstract

The mechanism of increased salt appetite and subsequent development of hypertension in response to deoxycorticosterone (DOC) administration in Sprague-Dawley rats is unclear. Recently it has been shown that the Long-Evans rat is resistant to DOC. A binding protein to DOC in brain cytosol is described with dissociation constant of 1.70–2.99 × 10^−l0M, and relative affinity for various steroids in the following sequence: deoxycorticosterone > corticosterone > aldosterone > progesterone > dexamethasone > testosterone. Brain distribution of this binding protein in Sprague-Dawley rats and Long-Evans rats was compared. Only in the hypothalamus was there a significant deficiency in the deoxycorticosterone-3H binding protein of the Long-Evans rat. Thus presence of this binding protein may be responsible for the ability of deoxycorticosterone to affect behavior by increasing salt appetite which may subsequently lead to hypertension in Sprague-Dawley rats. (Endocrinology94:1541, 1974)