Alpha 1-adrenoceptor blockade and altered renal alpha 2-adrenoceptors: a model(?) for the study of genetically altered alpha 2-adrenoceptors in @entity101 XXXX .

@entity3160 @entity8 @entity101 @entity35 @entity1372 @entity3159
@entity8 ( @entity8 )-induced @entity1372 retention is normally mediated by alpha 1-adrenoceptors. Clinically, chronic @entity3159 therapy increases rather than decreases @entity1372 retention. In preliminary studies, chronic @entity3159 (3 days, 3 mg/kg per day) increased renal alpha 2-adrenoceptor density (mean +/- s.e.m., 153 +/- 14 versus 209 +/- 11 fmol/mg protein) in normal @entity35 . We therefore postulated that following chronic @entity3159 treatment, alpha 2-adrenoceptors may mediate @entity8 -induced @entity1372 retention. The effect of chronic @entity3159 pretreatment on the alpha-adrenoceptor subtype mediating @entity8 -induced antinatriuresis was studied in the perfused @entity35 kidney. In control @entity35 , subpressor levels of @entity8 (approximately 1 Hz, 10 V, 1 ms) decreased @entity1372 and water excretion. @entity3159 28 nmol/l (alpha 1-blockade) reversed this effect of @entity8 . @entity3160 300 nmol/l (alpha 2-blockade) had no effect. In @entity35 treated with @entity3159 , @entity8 again decreased @entity1372 and water excretion. In these @entity35 , @entity3160 as well as @entity3159 was necessary to reverse the effects of @entity8 . Thus, following @entity3159 pretreatment postjunctional alpha 2- as well as alpha 1-adrenoceptors mediated @entity8 -induced antinatriuresis. A similar function of the elevated renal alpha 2-adrenoceptors in @entity101 in @entity35 could possibly explain the mechanism by which excess @entity1372 retention occurs and thereby the elevation of blood pressure.
