Key result
Pertussis toxin abolishes adenosine-mediated myocardial inhibition and triggers calcium overload with necrosis.
Why the study?
The role of pertussis toxin sensitive N proteins in mediating the inhibitory effects of adenosine on myocardial contraction and calcium currents during beta adrenergic stimulation was unclear.
Does pertussis toxin pretreatment abolish the inhibitory effects of adenosine on force of contraction and slow calcium inward current in guinea pig papillary muscles?
Population
Papillary muscles and hearts from guinea pigs
Comparison
Pretreatment with pertussis toxin vs control solvent alone
Design
Preclinical experimental study
Authors
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May implicate pertussis toxin-sensitive N proteins in calcium-mediated necrosis; hypothesis-generating for cardiomyopathy mechanisms, not yet clinically relevant.
Does pertussis toxin pretreatment abolish the inhibitory effects of adenosine on force of contraction and slow calcium inward current in guinea pig papillary muscles?
Pertussis toxin-sensitive N proteins mediate the inhibitory effects of adenosine on myocardial contraction and calcium current, and their uncoupling leads to myocardial necrosis and calcium overload, suggesting a mechanism for cardiomyopathy.
Böhm et al. (1988) studied this question. Pertussis toxin pretreatment vs. Control (solvent alone) was evaluated on Force of contraction, maximal rate of depolarisation, and myocardial necrosis. Pretreatment with pertussis toxin abolished the inhibitory effects of adenosine and PIA on myocardial contraction and calcium currents, and produced disseminated myocardial necrosis and calcium overload.
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