Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 33, Issue 3, Pages 561-573Publisher
ELSEVIER SCI LTD
DOI: 10.1006/jmcc.2000.1332
Keywords
adrenergic receptor; atrial natriuretic factor; isoproterenol; beta-galactosidase; luciferase; pertussis toxin
Categories
Funding
- NHLBI NIH HHS [HL62716, HL33107, HL59874, HL59139, HL37404, HL67724] Funding Source: Medline
- NIA NIH HHS [AG14121] Funding Source: Medline
Ask authors/readers for more resources
Myocardial P-adrenergic receptors (beta -ARs) consist of beta (1)- and beta (2)-subtypes, which mediate distinct signaling mechanisms. We examined which beta -AR subtype mediates cardiac hypertrophy. The beta (2)-subtype is predominant in nconatal rat cardiac myocytes (beta (1), 36% v beta (2), 64%), while the beta (1)-subtype predominates in the adult rat heart (59% v 41%). Stimulation of cultured cardiac myocytes in vitro with isoproterenol (ISO), an agonist for beta (1)- and beta (2)-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 beta (1)-AR antagonist, betaxolol, but not by a beta (2)-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 beta -AR stimulated hypertrophy is mediated by the beta (1)-subtype and by a pertussis toxin-insensitive mechanism. (C) 2001 Academic Press.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available