出版社：Japan Society of Circulation Control in Medicine
摘要：We examined the effects of α2-adrenergic agonist, dexmedetomidine(DEX), on tetrodotoxin-resistant (TTX-r) Na+ currents using small-sized dorsal root ganglion(DRG) cells of the rats. Whole cell patch-clamp configuration was used. After control Na+ current was recorded, DEX was added to the extracellular solution. Yohimbine and prazosin were used to differentiate the contribution of α2-adrenergic receptor from that of α1-adrenergic receptor. The peak TTX-r Na+ currents were significantly and dose dependently inhibited by DEX(p<0.05). Yohimbine attenuated the suppressive effects of DEX on TTX-r Na+ currents, while prazosin did not alter the effects of DEX. Thus, DEX inhibited TTX-r Na+ currents by way of α2-adrenergic receptors but not α1-adrenergic receptors. Therefore, it is suggested that DEX has an inhibitory effect on TTX-r Na+ channels through α2-adrenergic receptors.
