Key result
Chronic beta1-adrenoceptor blockade with atenolol was associated with a 65% higher G(s)alpha activity in human atrial myocardium compared to non-beta-blocked patients (78.2 vs 47.3; P=0.02).
Why the study?
Does chronic selective beta1-blocker treatment enhance stimulatory G-protein function in human atrial myocardium compared to no beta-blocker treatment?
Population
Human atrial myocardium from patients treated with chronic selective beta1-blockers and non-beta-blocked…
Comparison
Chronic selective beta1-adrenoceptor blocker… vs No beta-blocker treatment
Design
Preclinical
Authors
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May underlie Gs-coupled receptor hypersensitivity during beta1-blockade; leaves open effects on atrial arrhythmia risk.
Observational (n=15)
Does chronic selective beta1-blocker treatment enhance stimulatory G-protein function in human atrial myocardium compared to no beta-blocker treatment?
Effect estimate: 65% higher
Absolute Event Rate: 78.2% vs 47.3%
p-value: p=0.02
Chronic selective beta1-blockade enhances Gsalpha function in human atrium, which may account for the hypersensitivity of beta2AR and other Gs-coupled receptors during beta1-blockade.
Wang et al. (1999) conducted an observational in Patients providing human atrial myocardium samples (n=15). Chronic selective beta1-adrenoceptor blocker (atenolol) treatment vs. Non-beta-blocked patients was evaluated on G(s)alpha activity upon 10(-4) M GTPgammaS stimulation (pmol cyclic AMP mg(-1) min(-1) 10(-3)) (65% higher, p=0.02). Chronic beta1-adrenoceptor blockade with atenolol was associated with a 65% higher G(s)alpha activity in human atrial myocardium compared to non-beta-blocked patients (78.2 vs 47.3; P=0.02).
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