β-adrenergic cardiac hypertrophy is mediated primarily by the β1-subtype in the rat heart

Carmine Morisco, David C. Zebrowski, Dorothy E. Vatner, Stephen F. Vatner, Junichi Sadoshima

Research output: Contribution to journalArticlepeer-review

119 Scopus citations

Abstract

Myocardial β-adrenergic receptors (β-ARs) consist of β1- and β2-subtypes, which mediate distinct signaling mechanisms. We examined which β-AR subtype mediates cardiac hypertrophy. The β2-subtype is predominant in neonatal rat cardiac myocytes (β1, 36% ν β2, 64%), while the β1-subtype predominates in the adult rat heart (59% ν 41%). Stimulation of cultured cardiac myocytes in vitro with isoproterenol (ISO), an agonist for β1- and β2-ARs, caused hypertrophy of myocytes along with increases in transcription of atrial natriuretic factor (ANF) and actin reorganization. All of these ISO-mediated myocyte responses in vitro were inhibited by a β1-AR antagonist, betaxolol, but not by a β2-AR antagonist. ICI 118551. Pertussis toxin failed to affect ISO-induced increases in total protein/DNA content and ANF transcription in vitro. ISO increased LV weight/body weight and ANF transcription in the adult rat in vivo, which were also inhibited by betaxolol but not by ICI 118551. These results suggest that β-AR stimulated hypertrophy is mediated by the β1-subtype and by a pertussis toxin-insensitive mechanism.

Original languageEnglish (US)
Pages (from-to)561-573
Number of pages13
JournalJournal of Molecular and Cellular Cardiology
Volume33
Issue number3
DOIs
StatePublished - 2001

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

Keywords

  • Adrenergic receptor
  • Atrial natriuretic factor
  • Isoproterenol
  • Luciferase
  • Pertussis toxin
  • β-Galactosidase

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