Open AccessCloning and expression of a rat cardiac delayed rectifier potassium channel.
Author(s) -
Markus Paulmichl,
Patricia E. Nasmith,
Renate Hellmiss,
Karen E. Reed,
Walter A. Boyle,
Jeanne M. Nerbonne,
Ernest G. Peralta,
David E. Clapham
Publication year - 1991
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.88.17.7892
Subject(s) - inward rectifier potassium ion channel , atrium (architecture) , tetraethylammonium , endocrinology , medicine , xenopus , potassium channel , complementary dna , ventricle , biology , tetraethylammonium chloride , potassium channel blocker , chemistry , western blot , microbiology and biotechnology , potassium , ion channel , biochemistry , receptor , gene , atrial fibrillation , organic chemistry
We have cloned a cDNA (designated RAK) coding for a delayed-rectifier K current (IRAK) from adult rat heart atrium and expressed it in Xenopus oocytes. RAK differs from the cloned rat brain K current, BK2 [McKinnon, D. (1989) J. Biol. Chem. 264, 8230-8236], by one amino acid at residue 411. RAK expressed in oocytes compares closely to the intrinsic adult rat atrial delayed-rectifier current measured by using whole-cell recording of single isolated cells. Northern blot analysis confirmed the presence of the channel in adult rat atrium, and to a lesser extent, in rat ventricle. IRAK activates with time constants ranging from 58 ms at -20 mV to 6 ms at +60 mV and does not show significant inactivation over 800 ms. It is blocked by 4-aminopyridine greater than barium much greater than tetraethylammonium chloride, which is similar to the relative potencies of these blockers on the native delayed rectifier current. We conclude that the main delayed rectifier K current in adult rat atria is virtually identical to a neuronal delayed rectifier, BK2.