English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background —Although tachycardia is commonly present in patients with congestive heart failure, its role in the development of congestive heart failure remains unclear. We studied the effect of rapid electrical stimulation of contraction on β-adrenergic receptor (β-AR) signal pathway in cultured cardiomyocytes of neonatal rats.Methods and Results —Contraction of cardiomyocytes was induced by electrical stimulation at 50 V with twice the threshold pulse width. β-ARs were identified by [3 H]CGP-12177 and [3 H]dihydroalprenolol. Electrical stimulation reduced cell-surface but not total β-AR density; the effect was dependent on pacing frequency (a reduction of 11%, 28%, and 18% in cells paced at 2.5, 3.0, and 3.3 Hz, respectively). This reduction was apparent at 3 hours, in contrast to reduced β-AR density after exposure to isoproterenol (ISP) for 1 hour. The fraction and inhibition constant of β-AR binding agonist with high affinity were not affected by rapid electrical stimulation. In cardiomyocytes paced at 3.0 Hz for 24 hours, the response to ISP decreased compared with unpaced cells, 142% versus 204% of baseline with 1 μmol/L ISP, whereas the responses to forskolin or acetylcholine were not different. Treatment of cardiomyocytes with 2,3-butanedione monoxime (10 mmol/L) or taxol (10 μmol/L) inhibited the rapid pacing–induced reduction in β-AR density.Conclusions —Our results suggest that contractile activity is involved in regulation of cardiac function by modulating the β-AR system independently of hemodynamic and neurohormonal factors. This may help to elucidate the role of mechanical stress in the development of heart failure.

Rapid Electrical Stimulation of Contraction Reduces the Density of β-Adrenergic Receptors and Responsiveness of Cultured Neonatal Rat Cardiomyocytes