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Vasodilatation induced by a new NO donor involve KCa channels activation and cell membrane hyperpolarization

This study aimed to investigate the role of K+ channels activation induced by the new NO donor cis‐[Ru(bpy)2(py)NO2](PF6) (PY). Vascular reactivity was studied in denuded rat aortic rings and efficacy (ME) and potency (pD2) of PY were analyzed. Concentration‐effect curves for the NO donor were constructed in phenylephrine (Phe) or 60 mM KCl‐contracted arteries. Efficacy and potency values were lower in KCl (ME 60.2±3.5%, pD2 5.86±0.09, n=6) than in Phe‐contracted aortic rings (ME 104.4±1.0%, pD2 6.54±0.07, n=5). TEA (1mM), which is considered selective for KCa channels inhibited the relaxation to PY in Phe‐contracted arteries (ME 93.1±1.9%, pD2 5.83±0.13, n=6). Only Ca2+‐activated (KCa) blocker Apamin (1μM) reduced the Hill slope of the curve to PY from 2.66±0.37 (n=5) to 1.33±0.15 (n=6), but it did not alter the potency or efficacy of PY. The blockade of K+ channels voltage‐dependent (Kv) and ATP‐sensitive (KATP) had no effect on the relaxation induced by PY. In order to assess the effect of PY on the membrane potential of smooth muscle cells we used Di‐4‐Anepps probe and laser scanning confocalmicroscopy. The addition of PY decreased the ratio of fluorescence of the dye, suggesting that PY causes aortic cells membrane hyperpolarization. In conclusion, the vasorelaxation induced by the new NO donor involves KCa channels activation and cell membrane hyperpolarization. Supported by FAPESP, CAPES and CNPq.