Senazodan (MCI 154) (hydrochloride), as a Ca 2+ sensitiser, shows inhibition effect on PDE III In Vitro Senazodan (hydrochloride) seems to affect directly the actin-myosin crossbridge kinetics, and increases myosin ATPase activity. Senazodan (hydrochloride) produces a concentration-dependent increase in tension development. Senazodan (hydrochloride) enhances Ca 2+ binding to myofilaments and to purified cardiac troponin C. Senazodan (hydrochloride) also enhances contractility in guinea-pig papillary muscles by inhibiting PDE III.Senazodan (0.1 nM~0.1 mM) (hydrochloride) shows that the contractile response of superior mesenteric arterie (SMA) to norepinephrine (NE) after hemorrhagic shock is significantly decreased as compared with the normal control group. Senazodan (0.01 mM) (hydrochloride) pretreatment prevents the effects of Ang II, and the concentration-response curve of Ca 2+ is shifted to the right as compared with Ang II-alone group. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Senazodan (0.1~2.0 mg/kg; left femoral vein catheterization infusion) (hydrochloride) decreases the pressor effect of norepinephrine (NE). Senazodan (0.1 mg/kg; i.v.) (hydrochloride) makes LVSP, IP, MC, and Lo all increased significantly, while heart rate is not obviously changed and left ventricular end-diastolic pressure (LVEDP) is reduced remarkably. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Wistar rats (200~250 g)Dosage: 0.1~2.0 mg/kg Administration: Left femoral vein catheterization infusion Result: Decreased the pressor effect of norepinephrine (NE). Animal Model: RabbitsDosage: 0.1 mg/kg Administration: I.v. Result: LVSP, IP, MC, and Lo all were increased significantly while heart rate was not obviously changed and left ventricular end-diastolic pressure (LVEDP) was reduced remarkably. Form:Solid IC50& Target:PDE III