PubMed:22572849 JSONTXT 7 Projects

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Id Subject Object Predicate Lexical cue
T1 108-266 DRI_Approach denotes We investigated the impairment of ATP-sensitive K(+) (K(ATP)) channels in aortic smooth muscle cells (ASMCs) from isoproterenol-induced hypertrophied rabbits.
T2 267-421 DRI_Approach denotes The amplitude of K(ATP) channels induced by the K(ATP) channel opener pinacidil (10 μM) was greater in ASMCs from control than from hypertrophied animals.
T3 422-524 DRI_Background denotes In phenylephrine-preconstricted aortic rings, pinacidil induced relaxation in a dose-dependent manner.
T4 525-679 DRI_Outcome denotes The dose-dependent curve was shifted to the right in the hypertrophied (EC(50): 17.80 ± 3.28 μM) compared with the control model (EC(50): 6.69 ± 2.40 μM).
T5 680-881 DRI_Background denotes 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.
T6 882-1209 DRI_Approach denotes Application of the calcitonin-gene related peptide (100 nM) and adenylyl cyclase activator forskolin (10 μM), 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.
T7 1210-1300 DRI_Outcome denotes Furthermore, PKA expression was not altered between the control and hypertrophied animals.
T8 1301-1378 DRI_Outcome denotes These results suggests that the decreased K(ATP) current amplitude and K(ATP)
T9 1410-1597 DRI_Outcome denotes 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.