Why the study?
Does pertussis toxin treatment improve beta-adrenoceptor responsiveness in isolated cardiac myocytes from failing human hearts and noradrenaline-treated guinea-pigs?
Population
Isolated cardiac myocytes from failing human myocardium, non-failing human myocardium, noradrenaline-treated…
Comparison
Pertussis toxin treatment vs Myocytes incubated in the absence of pertussis…
Design
Preclinical
Authors
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Remains preclinical in isolated myocytes; leaves open whether inhibitory G-protein inactivation restores beta-adrenoceptor responsiveness in heart failure.
Does pertussis toxin treatment improve beta-adrenoceptor responsiveness in isolated cardiac myocytes from failing human hearts and noradrenaline-treated guinea-pigs?
Inactivation of inhibitory G-proteins by pertussis toxin restores beta-adrenoceptor responsiveness in failing human and noradrenaline-treated guinea-pig cardiac myocytes, suggesting increased inhibitory G-protein activity contributes to desensitization in heart failure.
Brown et al. (1992) studied this question.
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