Pertussis toxin differentiates between α1- and α2-adrenoceptor-mediated inhibition of noradrenaline release from rat kidney cortex

Abstract

In slices of rat kidney cortex incubated in [ 3H]noradrenaline, the α 1-adrenoceptor agonist methoxamine (10 μM), the α 2-adrenoceptor agonist clonidine (0.1 μM), as well as adenosine (10 μM), inhibited the electrical stimulation-induced (S-I) outflow of radioactivity, at a stimulation frequency of 1 Hz. Prior treatment of rats with pertussis toxin (25 μg/kg i.v.) which abolished the negative inotropic effect of carbachol (10 μM) on isolated atria, prevented the inhibition caused by methoxamine, but not caused by clonidine or adenosine. At a stimulation frequency of 5 Hz, the α 2-adrenoceptor antagonist idazoxan (0.1 μM) and the prostaglandin synthesis indomethacin (10 μM) both facilatated the S-I outflow of radioactivity, and neither of these effects were altered by pertussis toxin. These results suggest that a pertussis toxin sensitive G-protein is involved in α 1-adrenoceptor inhibition of noradrenaline release, but not in α 2-adrenoceptor, adenosine or prostaglandin inhibition.