Figure 3. IKK2 contributes to diverse vascular contractile responses.

A, endothelium-denuded rat aortic rings were contracted by the indicated vasoconstrictors (1 µM PE, phenylephrine; 120 mM KCl, potassium chloride; 1 µM U-46619, a thromboxane A2 agonist; 1 µM calyculin A, a MLCP inhibitor), and then 30 µM SC-514 was added. A representative recording from at least three independent experiments is presented. B, endothelium denuded rat aortic rings were treated with ionomycin (1.5 µM) in calcium-free PSS for 30 minutes, and contracted with CaCl₂ (0.4 mM), and the IKK2 inhibitor SC-514 (100 µM) or vehicle was added. A representative result from four independent experiments is presented. C, endothelium denuded rat aortic rings were contracted by PE (1µM), and the IKK2 inhibitor SC-514 was added in an accumulative manner. Results were expressed as percentage of pre-contraction. D and E, phenylephrine (PE, 1 µM) pre-contracted endothelium denuded rat aortic rings were treated with IKK2 inhibitory or control peptide (the same peptides as in Fig. 2E and F. 50 µg/ml). The representative recordings (C) and the quantification data (D) are presented. n=3. *P<0.05 vs. control; student t-test. F, endothelium denuded rat aortic rings were contracted with calyculin A, followed by ML-9 (100µM) was added. After washing, the rings were contracted with PE again and followed by ML-9 (100µM). A representative result from three independent experiments is presented.