Alpha-adrenergic activation reduces junctional conductance in ventricular heart cells and interacts with the effects of beta-adrenergic stimulation.
Alpha-adrenergic activation may impair ventricular coupling; hypothesis-generating for beta-adrenergic interactions and arrhythmogenesis in vivo.
The influence of phenylephrine (10(-6) M) on the regulation of junctional conductance (gj) was investigated in heart-cell pairs isolated from the ventricles of adult rats. The results indicated that phenylephrine reduced gj by 45% (SEM, +/- 3.4; n = 20; p < 0.05) within 2 min of it's administration to the bath. The effect of phenylephrine was dose dependent and was abolished by prazosin (10(-6) M). Moreover, the activation of protein kinase C seems essential for the effect of phenylephrine on gj, because previous inhibition of protein kinase C reduced the effect of the drug. Norepinephrine (10(-6) M) or epinephrine (10(-6) M) increased gj by 56% (SEM, +/- 5.3; p < 0.05; n = 14) and 43.6% (SEM, +/- 4.1; n = 12; p < 0.05), respectively, and their effects were larger in the alpha 1-adrenergic receptor was blocked with prazosin. The results indicate that alpha-adrenergic activation reduces gj and interacts with the influence of beta-adrenergic stimulation on junctional conductance.
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Walmor C. De Mello (1997) studied this question.
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