SR33805 is a potent Ca 2+ channel antagonist, with EC 50 s of 4.1 nM and 33 nM in depolarized and polarized conditions, respectively. SR33805 blocks L-type but not T-type Ca 2+ channels. SR33805 can be used for the research of acute or chronic failing hearts
In Vitro
SR33805 (0.01-10 µM; 3 d) inhibits growth factor-induced proliferation of SMC (0.20 50<0.46 µM) in a dose-dependent manner. SR33805 (10 µM; 10 min) restores the myocardial infarction (MI)-altered cell shortening without affecting the Ca 2+ transient amplitude. SR33805 (10 µM) decreases the activity of recombinant PKA. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: Smooth muscle cells (SMC) Concentration: 0.01, 0.1, 1, 10 µM Incubation Time: 3 days Result: Inhibited in a dose-dependent manner FCS-, bFGF and PDGF-induced proliferation of porcine SMC with IC 50 s of 0.26±0.08, 0.46±0.1 and 0.20±0.04 µM, respectively.
In Vivo
SR33805 (20 mg/kg; a single i.p.) improves end-systolic strain and fractional shortening of MI hearts in rats. SR33805 (5 mg/kg/day; p.o. for 38 d) significantly reduces intimal hyperplasia in pigs. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male Wistar rats (5 weeks) are subjected to coronary artery ligatureDosage: 0.2, 2, 20 mg/kg Administration: A single i.p. injection Result: Increased significantly both end-systolic strain (ESS) and fractional shortening (FS) by about +38 and +26%, respectively at the dose of 20 mg/kg. Did not affect other contractile parameters.