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secretion in primary cultures of mouse cortical collecting
ducts
Institut National de la Santé et de la Recherche Médicale, 1 Unité 478 et 2 Unité 426, Institut Fédératif de Recherche 02, Faculté de Médecine Xavier Bichat, 75870 Paris, France
The role of
the cystic fibrosis transmembrane conductance regulator (CFTR) in the
renal cortical collecting duct (CCD) has not yet been fully elucidated.
Here, we investigated the effects of deamino-8-D-arginine
vasopressin (dDAVP) and isoproterenol (ISO) on NaCl transport in
primary cultured CCDs microdissected from normal [CFTR(+/+)] and
CFTR-knockout [CFTR(
/)] mice. dDAVP stimulated the benzamyl
amiloride (BAm)-sensitive transport of Na+ assessed by the
short-circuit current (Isc) method in both
CFTR(+/+) and CFTR(/) CCDs to a very similar degree. Apical
addition of 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) or
glibenclamide partially inhibited the rise in
Isc induced by dDAVP and ISO in BAm-treated
CFTR(+/+) CCDs, whereas dDAVP, ISO, and NPPB did not alter
Isc in BAm-treated CFTR(/) CCDs. dDAVP
stimulated the apical-to-basal flux and, to a lesser extent, the
basal-to-apical flux of 36Cl
in CFTR(+/+)
CCDs. dDAVP also increased the apical-to-basal
36Cl flux in CFTR(/) CCDs but not the
basal-to-apical 36Cl flux. These results
demonstrate that CFTR mediates the cAMP-stimulated component of
secreted Cl in mouse CCD.
cyclic adenosine monophosphate; kidney; epithelial sodium channel; cystic fibrosis transmembrane conductance regulator; cystic fibrosis
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