Chronic treatment with prazosin causes a subtype-specific increase in the α₁-adrenoceptor density of the stressed rat cerebral cortex

The effects of chronic treatment with prazosin and of immobilization stress on the α₁-adrenoceptor subtypes in rat cerebral cortex have been examined. Prazosin-treated rats were allowed free access to tap water containing two different concentrations of prazosin (16 or 156 mg L^-1) for 5 weeks. The mean plasma concentrations of prazosin were 5 ng mL^-1 in groups treated with a low dose and 8 or 14 ng mL^-1 in those treated with a high dose. Immobilization stress (2 h day^-1, 2 weeks) or chronic treatment with a low dose of prazosin caused no significant change in the affinity for [³H]prazosin or in the maximum number of α₁-adrenoceptor sites (B(max)). However, treatment with prazosin (low dose) combined with stress increased the density of α₁-adrenoceptors with low affinity for prazosin. Treatment with a high dose of prazosin increased the density of α(1L)-adrenoceptors, irrespective of stress loading. The densities of α(1A)- and α(1B)-adrenoceptors with high affinity for prazosin were increased only after treatment with a high dose of prazosin in combination with stress. These results indicate that three distinct α₁-adrenoceptor subtypes, α(1A), α(1B) and α(1L), might be affected differently by treatment with prazosin and by stress.