Alterations of [beta]3-adrenoceptors expression and their myocardial functional effects in physiological model of chronic exercise-induced cardiac hypertrophy

• Published in: Molecular and cellular biochemistry Vol. 300; no. 1-2; p. 69
• Main Authors: Barbier, J, Rannou-bekono, F, Marchais, J, Tanguy, S, Carré, F
• Format: Journal Article
• Language: English
• Published: New York Springer Nature B.V 01.06.2007
• Subjects: Gene expression; Rodents
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-006-9370-9

Physical training induces cardiovascular autonomic nervous system regulation adaptations, which could result from β adrenergic receptor (AR) modifications. Among them, β^sub 3^AR alterations have been recently reported but their functional effect remained to discuss. To explain the β^sub 3^ AR gene expression in relation to function, we simultaneously studied the left ventricle (LV) β^sub 3^ AR mRNA and protein levels and the myocardial functional effects of a β^sub 3^ AR agonist following physical training. Forty rats were assigned to either a control (C; N = 20) or a trained (T; N = 20) group. The treadmill running protocol was performed for 8 weeks. Histological measurements on LV slices were quantified. The β^sub 3^ AR mRNA abundance was studied with RT-PCR and β^sub 3^ AR protein density with Western-Blot analysis. Myocardial functional effects of a β^sub 3^ AR agonist, BRL37344 (10^sup -8^ M), were studied in Langendorff-perfused hearts. Histological data confirmed the adapted patterns of the physiological cardiac hypertrophy observed in T (P < 0.01), with a significant increase in arteries density (P < 0.01) and an unchanged collagen concentration. The β^sub 3^ AR protein density was increased in T (154 ± 38% in T vs. 100 ± 24% in C; P < 0.05), but no change was noted concerning the β^sub 3^ AR mRNA level. After BRL37344 perfusion LVDP, +dP/dT and -dP/dT, in C (P < 0.01), and only +dP/dT in T (P < 0.05) were decreased. Moreover, all LV hemodynamic parameters were more altered after BRL37344 in C than in T (P < 0.01). Thus, in this physiological model of cardiac hypertrophy, an increase of β^sub 3^ AR density without β^sub 3^ AR mRNA alteration was observed. Classical negative myocardial lusitropic and inotropic effects induced by a specific agonist of β^sub 3^ AR were diminished in trained rats.[PUBLICATION ABSTRACT]