Fig. 7: Schematic representation of the functional roles of TRPC3 and NCX1 in bladder SMCs.

The influx of Na⁺ and Ca²⁺ into bladder SMCs was increased through TRPC3 in DO rats. Furthermore, TRPC3 functionally interacted with NCX1 in bladder SMCs. TRPC3 activated the reverse mode of NCX1 by elevating Na⁺ levels in the subplasmalemmal space, thereby promoting Ca²⁺ entry into bladder SMCs in DO rats. As a consequence, three subplasmalemmal Na⁺ ions were transported out of the cell via TRPC3 to allow the entry of one Ca²⁺ ion into the cytoplasm through the reverse mode of NCX1 in bladder SMCs. The synergistic effects of TRPC3 and NCX1 significantly increased the [Ca²⁺]_i in bladder SMCs, which may have consequently contributed to DO.