Why the study?
Does tricyclohexyltin hydroxide inhibit beta-adrenergic stimulated calcium pump activity in rat cardiac sarcoplasmic reticulum?
Does tricyclohexyltin hydroxide inhibit beta-adrenergic stimulated calcium pump activity in rat cardiac sarcoplasmic reticulum?
Tricyclohexyltin hydroxide inhibits the cardiac sarcoplasmic reticulum calcium pump, potentially leading to altered calcium fluxes and cardiac dysfunction.
May indicate cardiotoxicity risk via altered calcium fluxes; leaves open relevance to human cardiac dysfunction.
The effects of tricyclohexyltin hydroxide (Plictran), an organotin acaricide, on 45Ca2+ uptake and Ca2+ ATPase were studied in vitro and in vivo in rat heart ventricular membrane vesicles, primarily sarcoplasmic reticulum. There was a concentration dependent inhibition of both 45Ca2+ uptake and Ca2+ ATPase in vivo as well as in vitro. Isoproterenol, a beta-adrenergic agonist, stimulated 45Ca2+ uptake and Ca2+ ATPase of sarcoplasmic reticulum and this was also inhibited by Plictran. Since cardiac relaxation is mediated by beta-adrenergic stimulation via Ca+ uptake by sarcoplasmic reticulum, the inhibition of calcium pump activity by Plictran may result in alterations in cardiac Ca2+ fluxes leading to cardiac dysfunction.
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Sahib et al. (1987) studied this question.
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