Stugeron Mechanism of Action

Pharmacology: In vitro and in vivo experiments have shown cinnarizine to reduce smooth muscle contractions induced by various vasoactive agents (histamine, angiotensin, bradykinin, nicotine, acetylcholine, adrenaline, noradrenaline, BaCl₂) and by KCl depolarization. Specific anticonstrictor activities were observed when vascular smooth muscles were used. Cinnarizine acts on the contractile response of depolarized smooth muscle fibres by selectively inhibiting the calcium influx into depolarized cells and thereby reducing the availability of free Ca⁺⁺ ions for the induction and maintenance of contraction. Cinnarizine is almost non-toxic and does not impede any of the important physiological functions (CNS, respiratory and circulatory function).
Pharmacokinetics: Isotope-labelled cinnarizine given to rats was found to be rapidly absorbed from the gastrointestinal tract and within 1-hr peak radioactivity levels were found in the blood, liver, kidneys, heart, spleen, lungs and brain. Extensive metabolization occurred within ½ hr of treatment and after 32 hrs, tissue drug levels were negligible. The drug was metabolized, especially by N-dealkylation. Approximately ²/₃ of the radioactive metabolites were excreted in the faeces, and ¹/₃ in the urine. Excretion was virtually accomplished within 5 days following administration.