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1 Division of Pediatric Nephrology, Department of Pediatrics, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029-6574; 2 Renal Division, Department of Medicine, University of Pennsylvania, Philadelphia 19104-6144; and 3 Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15213
K+ secretion by the
cortical collecting duct (CCD) is stimulated at high flow rates.
Patch-clamp analysis has identified a small-conductance secretory
K+ (SK) and a high-conductance Ca2+-activated
K+ (maxi-K) channel in the apical membrane of the CCD. The
SK channel, encoded by ROMK, is believed to mediate baseline
K+ secretion. The role of the stretch- and
Ca2+-activated maxi-K channel is still uncertain. The
purpose of this study was to identify the K+ channel
mediating flow-dependent K+ secretion in the CCD. Segments
isolated from New Zealand White rabbits were microperfused in the
absence and presence of luminal tetraethylammonium (TEA) or
charybdotoxin, both inhibitors of maxi-K but not SK channels, or
apamin, an inhibitor of small-conductance maxi-K+ channels.
Net K+ secretion and Na+ absorption were
measured at varying flow rates. In the absence of TEA, net
K+ secretion increased from 8.3 ± 1.0 to 23.4 ± 4.7 pmol · min
1 · mm1
(P < 0.03) as the tubular flow rate was increased from
0.5 to 6 nl · min1 · mm1.
Flow stimulation of net K+ secretion was blocked by luminal
TEA (8.2 ± 1.2 vs. 9.9 ± 2.7 pmol · min1 · mm1 at 0.6 and 6 nl · min1 · mm1 flow
rates, respectively) or charybdotoxin (6.8 ± 1.6 vs. 8.3 ± 1.6 pmol · min1 · mm1 at 1 and
4 nl · min1 · mm1 flow
rates, respectively) but not by apamin. These results suggest that
flow-dependent K+ secretion is mediated by a maxi-K
channel, whereas baseline K+ secretion occurs through a
TEA- and charybdotoxin-insensitive SK (ROMK) channel.
principal cell; intercalated cell; ROMK; epithelial sodium channels; charybdotoxin; apamin
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