| First Author | Koh SD | Year | 2001 |
| Journal | J Biol Chem | Volume | 276 |
| Issue | 47 | Pages | 44338-46 |
| PubMed ID | 11560940 | Mgi Jnum | J:72776 |
| Mgi Id | MGI:2153583 | Doi | 10.1074/jbc.M108125200 |
| Citation | Koh SD, et al. (2001) TREK-1 Regulation by Nitric Oxide and cGMP-dependent Protein Kinase. AN ESSENTIAL ROLE IN SMOOTH MUSCLE INHIBITORY NEUROTRANSMISSION. J Biol Chem 276(47):44338-46 |
| abstractText | Potassium channels activated by membrane stretch may contribute to maintenance of relaxation of smooth muscle cells in visceral hollow organs. Previous work has identified K(+) channels in murine colon that are activated by stretch and further regulated by NO-dependent mechanisms. We have screened murine gastrointestinal, vascular, bladder, and uterine smooth muscles for the expression of TREK and TRAAK mRNA. Although TREK-1 was expressed in many of these smooth muscles, TREK-2 was expressed only in murine antrum and pulmonary artery. TRAAK was not expressed in any smooth muscle cells tested. Whole cell currents from TREK-1 expressed in mammalian COS cells were activated by stretch, and single channel recordings showed that the stretch-dependent conductance was due to 90 pS channels. Sodium nitroprusside (10(-6) or 10(-5) m) and 8-Br-cGMP (10(-4) or 10(-3) m) increased TREK-1 currents in perforated whole cell and single channel recordings. Mutation of the PKG consensus sequence at serine 351 blocked the stimulatory effects of sodium nitroprusside and 8-Br-cGMP on open probability without affecting the inhibitory effects of 8-Br-cAMP. TREK-1 encodes a component of the stretch-activated K(+) conductance in smooth muscles and may contribute to nitrergic inhibition of gastrointestinal muscles. |
