Senazodan hydrochloride (Senazodan HCl) is a Ca2+ sensitizer and phosphodiesterase 3 (PDE3) inhibitor used in the study of cardiovascular diseases.

Senazodan hydrochloride appears to modulate actin-myosin cross-bridge dynamics and promote myosin ATPase activity [1].
Senazodan hydrochloride increases tonogenesis in a concentration-dependent manner while enhancing the binding capacity of calcium ions (Ca²⁺) to myofilaments as well as purified cardiac troponin C. The binding capacity of calcium ions to myofilaments is also enhanced by Senazodan hydrochloride. In addition, cenazolone hydrochloride improves contractile properties of guinea pig papillary muscle by inhibiting phosphodiesterase III (PDE III) [2].
Senazodan hydrochloride attenuated the contractile response induced by norepinephrine (NE) on the superior mesenteric artery (SMA) after hemorrhagic shock over the concentration range of 0.1 nM to 0.1 mM, which was significantly reduced compared to normal controls. 0.01 mM Senazodan hydrochloride pretreatment was able to inhibit the contraction of angiotensin II (Ang II) in guinea pigs. The effect of angiotensin II (Ang II) was significantly shifted to the right of the calcium concentration-response curve, which was more prominent in the Ang II group compared to the Ang II group alone. [3]

0.1 to 2.0 mg/kg Senazodan hydrochloride infused through a femoral vein catheter reduces the antihypertensive effect of norepinephrine (NE). [3]
Intravenous infusion of 0.1 mg/kg Senazodan hydrochloride significantly elevated left ventricular systolic pressure (LVSP), myocardial contractility (IP), myocardial contractility (MC), and left ventricular output (Lo) without significant changes in heart rate. Meanwhile, left ventricular end-diastolic pressure (LVEDP) was significantly decreased. [4]