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Park WS, Hong DH, Son YK, Kim MH, Jeong SH, Kim HK, Kim N, Han J. Alteration of ATP-sensitive K+ channels in rabbit aortic smooth muscle during left ventricular hypertrophy. Am J Physiol Cell Physiol 303: C170-C178, 2012. First published May 9, 2012; doi:10.1152/ajpcell.00041.2012.-We investigated the impairment of ATP-sensitive K+ (K-ATP) channels in aortic smooth muscle cells (ASMCs) from isoproterenol-induced hypertrophied rabbits. The amplitude of KATP channels induced by the K-ATP channel opener pinacidil (10 mu M) was greater in ASMCs from control than from hypertrophied animals. In phenylephrine-preconstricted aortic rings, pinacidil induced relaxation in a dose-dependent manner. The dose-dependent curve was shifted to the right in the hypertrophied (EC50: 17.80 +/- 3.28 mu M) compared with the control model (EC50: 6.69 +/- 2.40 mu M). Although the level of Kir6.2 subtype expression did not differ between ASMCs from the control and hypertrophied models, those of the Kir6.1 and SUR2B subtypes were decreased in the hypertrophied model. Application of the calcitonin-gene related peptide (100 nM) and adenylyl cyclase activator forskolin (10 mu M), which activates protein kinase A (PKA) and consequently K-ATP channels, induced a K-ATP current in both control and hypertrophied animals; however, the K-ATP current amplitude did not differ between the two groups. Furthermore, PKA expression was not altered between the control and hypertrophied animals. These results suggests that the decreased K-ATP current amplitude and K-ATP channel-induced vasorelaxation in the hypertrophied animals were attributable to the reduction in K-ATP channel expression but not to changes in the intracellular signaling mechanism that activates the K-ATP current.
- 出版日期2012-7
