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Fig. 5. A,a: effect of 20-HETE on hypoxia-induced activation of a 238-pS KCa single-channel current in rat cerebral arterial muscle cells. Single-channel KCa currents were recorded from cell-attached patches at a patch potential of +40 mV using symmetrical KCl (145 mM) solution. Hypoxia (<2% O2) significantly increased the openings (A,a) or NPo (A,b) of the 238-pS KCa single-channel current recorded in rat cerebral arterial muscle cells, which was attenuated in the presence of exogenously added 20-HETE (100 nM) to the hypoxic solution (P < 0.05; n = 9). Vertical lines represent means ± SE. P < 0.05 from the *normoxic and the #hypoxic condition. B,a: effects of inhibition of CYP 4A  -hydroxylase on the hypoxia-induced increased openings (B,a) and NPo (B,b) of the 238-pS single-channel KCa current. Pretreatment of the cells with 17-ODYA, suicide substrate inhibitor of the CYP 4A -hydroxylase (17-ODYA; 5 µM for 15 min) significantly increased the NPo of the 238-pS KCa single-channel current recorded at a patch potential of +40 mV using symmetrical KCl (145 mM) solution, an effect that was not enhanced further by hypoxic superfusion of the cells in the continuous presence of 5 µM 17-ODYA (<2% O2) (P > 0.05, n = 6). Vertical lines represent means ± SE. *Significant difference (P < 0.05) from the control.
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