Why the study?
Does β3-adrenoceptor deficiency alter nitric oxide-dependent inhibition of β-adrenergic-stimulated myocardial contractility in mice?
Population
Preclinical model: mice with homozygous β3-adrenoceptor deletion mutations, wild-type FVB mice, and…
Comparison
Isoproterenol infusion with or without NOS… vs Wild-type mice receiving the same infusions, and…
Design
Preclinical
Authors
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β3-NO negative feedback limits murine β-adrenergic inotropy; human relevance and therapeutic targeting remain untested.
Does β3-adrenoceptor deficiency alter nitric oxide-dependent inhibition of β-adrenergic-stimulated myocardial contractility in mice?
The β3-adrenoceptor plays a critical role in mediating nitric oxide-dependent negative feedback over β-adrenergic-stimulated myocardial contractility.
Varghese et al. (2000) studied this question.
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