Key result
In cultured rat ventricular myocytes, pertussis toxin markedly attenuated norepinephrine-stimulated inositol phosphate formation, establishing a role for a 41,000-dalton pertussis toxin substrate.
Why the study?
Does pertussis toxin inhibit norepinephrine-stimulated phosphatidylinositol hydrolysis in cultured rat ventricular myocytes?
Does pertussis toxin inhibit norepinephrine-stimulated phosphatidylinositol hydrolysis in cultured rat ventricular myocytes?
A 41,000-dalton pertussis toxin substrate plays a role in coupling the alpha 1-adrenergic receptor to phosphoinositol hydrolysis in myocardial cells.
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In vitro myocyte data on alpha1-adrenergic PI hydrolysis leave open pertussis toxin effects on chronotropy in vivo; hypothesis-generating only.
Steinberg et al. (1987) studied this question. Pertussis toxin was evaluated on Inositol phosphate (IP1) formation. In cultured rat ventricular myocytes, pertussis toxin markedly attenuated norepinephrine-stimulated inositol phosphate formation, establishing a role for a 41,000-dalton pertussis toxin substrate.
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