Plasma immunoreactive atrial natriuretic factor is inhibited by selective blockade of alpha 2-adrenergic receptors in conscious Sprague-Dawley rats.

Effects of alpha 2-adrenergic receptors and calcium channel blockade on basal and clonidine-stimulated immunoreactive atrial natriuretic factor (IR-ANF) in conscious Sprague-Dawley rats were evaluated. Clonidine was injected intravenously (i.v.) in a dose of 50 micrograms. Yohimbine and verapamil were used as a pretreatment, with clonidine in a dose of 50 micrograms and 0.5 mg respectively. The effects of yohimbine (1, 20, 50 micrograms) and verapamil (0.5 mg) on basal IR-ANF were also studied. Plasma IR-ANF was measured by radioimmunoassay with prior extraction on heat-activated Vycor glass. Clonidine injection in a dose of 50 micrograms caused a marked increase of plasma IR-ANF from 34.0 +/- 7.0 pg/ml (mean +/- S.E.M.) to 457.1 +/- 66.3 pg/ml. Clonidine-stimulated ANF secretion was partially inhibited by yohimbine from 457.1 +/- 66.3 pg/ml (mean +/- S.E.M.) to 99.9 +/- 23.1 pg/ml. Moreover, yohimbine in highest doses (50 micrograms) decreased the basal plasma IR-ANF from 34.0 +/- 7.0 pg/ml (means +/- S.E.M.) to 6.8 +/- 3.6 pg/ml. Verapamil did not alter basal and clonidine stimulated IR-ANF. These results indicate the important role played by alpha 2-adrenergic receptors in mediating ANF release.