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Inhibition of β‐adrenergic stimulated calcium pump of rat cardiac sarcoplasmic reticulum by tricyclohexyltin hydroxide
Author(s) -
Sahib I. Kabeer Ahammed,
Desaiah D.
Publication year - 1987
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290050211
Subject(s) - endoplasmic reticulum , ryanodine receptor 2 , calcium , adrenergic , chemistry , medicine , endocrinology , calcium pump , calcium hydroxide , biophysics , pharmacology , microbiology and biotechnology , biochemistry , biology , enzyme , ryanodine receptor , atpase , receptor
The effects of tricyclohexyltin hydroxide (Plictran), an organotin acaricide, on 45 Ca 2+ uptake and Ca 2+ 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 45 Ca 2+ uptake and Ca 2+ ATPase in vivo as well as in vitro . Isoproterenol, a β‐adrenergic agonist, stimulated 45 Ca 2+ uptake and Ca 2+ ATPase of sarcoplasmic reticulum and this was also inhibited by Plictran. Since cardiac relaxation is mediated by β‐adrenergic stimulation via Ca + uptake by sarcoplasmic reticulum, the inhibition of calcium pump activity by Plictran may result in alterations in cardiac Ca 2+ fluxes leading to cardiac dysfunction.
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