VASOPRESSIN V1A AND V2 RECEPTOR MESSENGER-RNA IN DEOXYCORTICOSTERONE ACETATE SALT HYPERTENSION IN THE RAT

1. Vasopressin V1a and V2 receptors are differentially regulated in de oxycorticosterone acetate-salt hypertension. This paper investigated w hether the changes were due to transcription changes in receptor mRNA assessed by in situ hybridization histochemistry Giver V1a receptor) a nd by reverse transcription-polymerase chain reaction (kidney V1a and V2 receptor). 2. Systolic blood pressure and plasma vasopressin levels were significantly elevated in deoxycorticosterone acetate-salt rats (n = 24) compared with water-control (n = 28) and salt-control rats (n = 28) (P < 0.001), Plasma sodium was elevated in deoxycorticosterone acetate-salt rats compared with both control groups (P < 0.01) and pla sma osmolality was elevated in deoxycorticosterone acetate-salt rats c ompared with water-control rats (P < 0.05). 3. Binding kinetic studies demonstrated downregulation of liver V1a and kidney V2 receptors in d eoxycorticosterone acetate-salt rats compared with water-control and s alt-control rats (P < 0.05), This was not associated with any change i n Liver V1a receptor mRNA (P = 0.95), or in kidney V1a (P = 0.79) or V 2 receptor mRNA (P = 0.96). 4. In deoxycorticosterone acetate-salt hyp ertension, downregulation of liver V1a and kidney V2 receptors occurs in the setting of stable vasopressin gene transcription, These results suggest that changes in receptor processing may be responsible for th e differential regulation of vasopressin receptors that occurs in deox ycorticosterone acetate-salt hypertension.