August 1, 2003British Journal of PharmacologyOpen Access

β‐adrenoceptor activation plays a role in the reverse rate‐dependency of effective refractory period lengthening by dofetilide in the guinea‐pig atrium, in vitro

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Structured PICO

Population

Guinea-pig left atrial myocardium and right ventricular papillary muscles of rabbits and guinea-pigs, in vitro

Intervention

Dofetilide (100 nM) combined with beta-adrenoceptor activation (isoproterenol 10 nM), beta-adrenoceptor blockade (metoprolol 1 micro M, atenolol 3 micro M, propranolol 300 nM), or catecholamine depletion (reserpine 5 mg/kg i.p. 24h pretreatment)

Comparator

Control conditions without beta-adrenoceptor modulators across different pacing rates (3, 2, and 1 Hz)

Outcome

Effective refractory period (ERP) lengtheningsurrogate

Rate-dependent noradrenaline release and subsequent beta-adrenoceptor activation contribute to the reverse rate-dependent ERP prolongation caused by I(Kr) blockers in guinea-pig atrial myocardium.

Discussion

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Implication

Beta-blockade may modulate IKr blocker effects on atrial ERP in guinea pigs; leaves open relevance to human antiarrhythmic therapy.

Cite This Study

Kovács et al. (2003) studied this question.

synapsesocial.com/papers/6a72b172a528af2d65c4810d https://doi.org/10.1038/sj.bjp.0705395

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β‐adrenoceptor activation plays a role in the reverse rate‐dependency of effective refractory period lengthening by dofetilide in the guinea‐pig atrium, in vitro

Structured PICO

Discussion

Implication

Cite This Study

β‐adrenoceptor activation plays a role in the reverse rate‐dependency of effective refractory period lengthening by dofetilide in the guinea‐pig atrium, in vitro

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider