“… 20 Both L- and N-type VGCCs are known to be present in the detrusor and take part in detrusor muscle contractility. 28 , 29 Hence, in the context of the current study, GV-58 causes increased detrusor muscle contractility by stimulating release of acetylcholine from parasympathetic nerve terminals, hence overcoming the relaxant effect of cilnidipine. 30 At the concentration of GV-58 used in the current study (6.8 µM), there is evidence from previous studies that it could have opened N-type VGCC.…”