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. 2008 Nov 12;296(2):R289–R298. doi: 10.1152/ajpregu.90656.2008

Fig. 6.

Fig. 6.

Membrane depolarization, reactive oxygen species (ROS) generation, and nitric oxide (NO) production in isolated pressurized cerebral arteries of ZO and ZL rats before and after diazoxide (100 μmol/l) administration.A: fluorescence images of the mitochondrial membrane potential-sensitive dye tetramethylrhodamine ethyl ester (TMRE) in ZL (top) and ZO (bottom) arteries in the absence and presence of diazoxide. B: TMRE fluorescence response to diazoxide. Reduction of diazoxide-induced decrease in TMRE fluorescence in ZO compared with ZL arteries indicates reduced mitochondrial depolarization. C: fluorescence images of the ROS sensitive dye hydroethidine (HEt) in ZL (top) and ZO (bottom) arteries following diazoxide administration. D: HEt fluorescence response to diazoxide compared with vehicle. E: fluorescence images of the NO-sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate (DAF-FM) in ZL (top) and ZO (bottom) arteries in the absence and presence of diazoxide. F: DAF-FM fluorescence response to diazoxide compared with vehicle. Reduction of diazoxide-induced increase in HEt and DAF-FM fluorescence in ZO compared with ZL arteries indicates decreased generation of ROS and NO, respectively. *Significantly different from lean (P < 0.05).