Modulation of noradrenaline release in slices of rat kidney cortex through α1- and α2-adrenoceptors

Abstract

Slices of rat kidney cortex were incubated in [ 3H]noradrenaline, then placed in a flow cell and subjected to electrical field stimulation. At a stimulation frequency of 5 Hz, both the α 2-adrenoceptor antagonist idazoxan (0.1 μM) and the α 1-adrenoceptor antagonist prazosin (0.1 μM) significantly enhanced the stimulation-induced (S-I) outflow of radioactivity from the slice. However, neither clonidine (0.1 μM) nor methoxamine (10 μM), α 2- and α 1-agonists respectively, affected the S-I outflow of radioactivity at this stimulation frequency. At a lower stimulation frequency (1 Hz), the S-I outflow of radioactivity was not affected by idazoxan or prazosin, but was inhibited by both clonidine and methoxamine. The effect of clonidine was prevented by idazoxan (0.1 μM), but not by prazosin (0.1 μM). The effect of methoxamine was abolished by prazosin (0.1 μM), but not by idazoxan (0.1 μM). The inhibitory effect of methoxamine was not prevented by the prostaglandin synthesis inhibitor indomethacin (10 μM) or the adenosine receptor antagonist 8-phenyltheophylline (1 μM) and thus was not mediated by either prostaglandins or adenosine. The results suggest that both prejunctional α 1- and α 2- adrenoceptors are directly involved in modulation of noradrenaline release from the renal sympathetic nerves of the rat.