Previous studies reported the existence of both D-1- and D-2-like receptors
in the cortical collecting duct (CCD). However, especially with regard to
natriuresis, it remains controversial. In the present study, rabbit CCD was
perfused to characterize the receptor subtypes responsible for the tubular
actions. Basolateral dopamine (DA) induced a dose-dependent depolarization
of transepithelial voltage. Basolateral domperidone, a D-2-like receptor a
ntagonist, abolished depolarization, whereas SKF-81297, a D(1-)like recepto
r agonist, showed no significant change. In addition, bromocriptine, a D-2-
like receptor agonist, also caused depolarization, whereas SKF-81297, a D-1
-like receptor agonist, did not depolarize significantly. Moreover, RBI-257
, a D-4-specific antagonist, reversed the basolateral DA-induced depolariza
tion. In contrast to the basolateral side, luminal DA caused depolarization
via a D-1-like receptor; however the change was less than that for basolat
eral DA. For further evaluation, Na-22(+) flux (J(Na)) was measured to conf
irm the effect of DA on Na+ transport. Basolateral DA also caused a suppres
sion of J(Na), and this reaction was abolished by domperidone. These result
s suggested that the basolateral D-2-like receptor is mainly responsible fo
r the natriuretic action of DA in rabbit CCD.