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Background  Multiple studies have shown that an  NO ‐induced activation of vascular smooth muscle BK channels contributes to the  NO ‐evoked dilation in many blood vessels. In vivo,  NO  is released continuously.  NO  attenuates vessel constrictions and, therefore, exerts an anticontractile effect. It is unknown whether the anticontractile effect of continuously present  NO  is mediated by  BK  channels.    Methods and Results  This study tested the hypothesis that  BK  channels mediate the vasodilatory effect of continuously present  NO . Experiments were performed on rat and mouse tail and rat saphenous arteries using isometric myography and  FURA ‐2 fluorimetry. Continuously present  NO  donors, as well as endogenous  NO , attenuated methoxamine‐induced vasoconstrictions. This effect was augmented in the presence of the  BK  channel blocker iberiotoxin. Moreover, the contractile effect of iberiotoxin was reduced in the presence of  NO  donors. The effect of the  NO  donor sodium nitroprusside was abolished by an  NO  scavenger and by a guanylyl cyclase inhibitor. In addition, the effect of sodium nitroprusside was reduced considerably by a protein kinase G inhibitor, but was not altered by inhibition of H 2 S generation. Sodium nitroprusside attenuated the intracellular calcium concentration response to methoxamine. Furthermore, sodium nitroprusside strongly reduced methoxamine‐induced calcium influx, which depends entirely on L‐type calcium channels. It did not affect methoxamine‐induced calcium release.    Conclusions  In summary, this study demonstrates the following: (1) continuously present  NO  evokes a strong anticontractile effect on rat and mouse arteries; (2) the iberiotoxin‐induced augmentation of the effect of  NO  is associated with an  NO ‐induced reduction of the effect of iberiotoxin; and (3)  NO  evoked a reduction of calcium influx via L‐type calcium channels.

The Unexpected Role of Calcium‐Activated Potassium Channels: Limitation of NO‐Induced Arterial Relaxation