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Two K(+)‐selective conductances in single proximal tubule cells isolated from frog kidney are regulated by ATP.
Author(s) -
Robson L,
Hunter M
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp022046
Subject(s) - quinidine , pipette , chemistry , biophysics , patch clamp , membrane potential , potassium channel , channel blocker , electrophysiology , biochemistry , medicine , pharmacology , biology , receptor , calcium , organic chemistry
1. The whole‐cell and single channel patch clamp techniques were used to identify K(+)‐selective conductances in single proximal tubule cells isolated from frog kidney and to examine their ATP sensitivity. Whole‐cell currents were inhibited by the K+ channel inhibitors Ba2+ and quinidine in a dose‐dependent manner. Addition of Ba2+ alone, quinidine alone, or both inhibitors together revealed two separate conductances, one of which was blocked by both Ba2+ and quinidine (GBa)1, the other being sensitive to quinidine alone (Gquin). 2. With Na(+)‐containing Ringer solution in the bath and K(+)‐containing Ringer solution in the pipette, both currents were selective for K+ over Na+. The K+ : Na+ selectivity ratio of GBa was around 50:1, while that of Gquin was 4:1. In symmetrical KCl solutions GBa showed inward rectification, while Gquin demonstrated outward rectification. 3. In the absence of pipette ATP, both GBa and Gquin ran down over 10 min. However, when 2 mM ATP was included in the pipette GBa increased, while Gquin remained unchanged. 4. Single channel studies demonstrated that a basolateral K+ channel shared several of the characteristics of GBa. It was inhibited by both Ba2+ and quinidine, underwent run‐down in excised patches in the absence of ATP, and was activated by ATP. 5. We conclude that cells of the frog proximal tubule contain at least two distinct K(+)‐selective conductances, both of which are regulated by ATP, and which may be involved in pump‐leak coupling.