At a dose of 210 nmol/kg (0.1 mg/kg), Solifenacin diminishes bladder responses by 40% and completely suppresses them at 2100 nmol/kg (1 mg/kg). However, its effects on salivary and cardiac responses are minimal at 630 nmol/kg (0.3 mg/kg), achieving inhibition levels of 66% and 49%, respectively, at 2100 nmol/kg (1 mg/kg). Lower doses of 63 and 210 nmol/kg (0.03 and 0.1 mg/kg) result in a slight increase in saliva secretion^[1].

Solifenacin (0.01 to 0.3 mg/kg intravenously) increases bladder capacity and voided volume in a dose-dependent manner beginning at 0.03 mg/kg intravenously. However, it has no impact on residual volume or micturition pressure at any of the doses tested^[2].

Solifenacin is a novel muscarinic receptor antagonist characterized by pKis of 7.6±0.056 for M1 receptors, 6.9±0.034 for M2 receptors, and 8.0±0.021 for M3 receptors. In studies involving murine submandibular gland cells, the effects of 100 nM Solifenacin and oxybutynin on Ca2+ mobilization induced by various doses of carbachol (CCh) are investigated. Unlike oxybutynin, which exhibits insurmountable antagonism, Solifenacin does not cause a parallel shift in the CCh dose-activation curve. The pKb values are determined to be 7.4±0.17 for Solifenacin and 8.8±0.21 for oxybutynin^[1].