Beta adrenergic modulation of cardiac rhythm in a rat model of altered sympathetic neural development

Susan F. Steinberg, Tove S. Rosen, Gabriella Malfatto, Michael R. Rosen

Research output: Contribution to journalArticlepeer-review


We previously have shown that treatment of neonatal rats (days 1-10) with Nerve Growth Factor (NGF) or its antibody (Ab) modifies α-adrenergic receptor-effector coupling, such that innervated hearts at day 10 show high levels of a 41 kDa GTP regulatory protein (G protein) that is a substrate for pertussis toxin and that links the α1-receptor to the Na K pump. This receptor-effector pathway results in α adrenergic-induced decreases in automaticity. In contrast, non-innervated hearts at day 10 show lower levels of the pertussis toxin sensitive G-protein and increases in automaticity induced by α-agonist. We now report the effects of administration of NGF, Ab or placebo on β-adrenergic receptor-effector coupling in neonatal rats. Rats were administered NGF, Ab or placebo on days 1-10 of life. On day 10, the β-receptor number and affinity and the stimulatory G-protein, Gs, were equivalent across groups. Moreover, the ventricular automatic response to β-adrenergic receptor stimulation was equivalent across groups suggesting there was no change in receptor-effector coupling as a result of the difference in innervation. These results on β-adrenergic receptor-effector coupling considered in light of our prior studies on α-adrenergic coupling suggest that the development of sympathetic innervation is more a determinant of α than β adrenergic modulation of ventricular rhythm.

Original languageEnglish
Pages (from-to)47-52
Number of pages6
JournalJournal of Molecular and Cellular Cardiology
Issue numberSUPPL. 1
Publication statusPublished - 1991


  • Automaticity
  • GTP regulatory proteins
  • Nerve growth factor and antibody
  • Receptor-effector coupling

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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