Inotropy and L‐type Ca2+current, activated by β1‐ and β2‐adrenoceptors, are differently controlled by phosphodiesterases 3 and 4 in rat heart

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Population

Isolated tissues (sinoatrial, left atrial, and ventricular) and cells from Wistar rats

Comparison

PDE3 inhibitor cilostamide and PDE4 inhibitor… vs Responses to-catecholamines without PDE inhibitors

Design

Preclinical

Authors

Discussion

Hypothesis-generating for PDE isoform-specific beta-adrenoceptor regulation in rat heart; leaves open translation to human cardiac physiology.

Population

Isolated tissues (sinoatrial, left atrial, and ventricular) and cells from Wistar rats

Intervention

PDE3 inhibitor cilostamide (300 nmol/L) and PDE4 inhibitor rolipram (1 micromol/L) administered with (-)-noradrenaline or (-)-adrenaline

Comparator

Responses to (-)-catecholamines without PDE inhibitors

Outcome

Sinoatrial beating rate, left atrial and ventricular contractile force, and L-type Ca2+ current (I(Ca-L))surrogate

PDE3 and PDE4 differentially regulate beta1- and beta2-adrenoceptor-mediated inotropic effects and calcium currents in the rat heart.

Christ et al. (2008) studied this question.

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Hypothesis-generating for PDE isoform-specific beta-adrenoceptor regulation in rat heart; leaves open translation to human cardiac physiology.