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1.
DNA Cell Biol ; 23(9): 586-91, 2004 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-15383178

RESUMEN

The role of A- and B-type natriuretic peptides (ANP and BNP) in cardiac pathophysiology are of increasing interest. Isolated neonatal mouse cardiac myocytes express increased levels of ANP mRNA in the absence of growth factors in culture. Expression of ANP and BNP mRNA has not been studied in isolated adult mouse cardiac myocytes (AMCM). We examined expression of ANP and BNP mRNA in isolated AMCM with and without stimulation with beta-adrenergic receptor agonists and antagonists. AMCM were isolated and maintained in culture for 24-48 h with and without stimulation with the beta-adrenergic receptor agonist isoproterenol (Iso), the beta1-antagonist CGP20712A (CGP), or the beta2-antagonist ICI-118,551 (ICI). Northern blot analysis was performed using probes for mouse ANP and BNP mRNA. TUNEL assay was performed after beta-adrenergic receptor stimulation of AMCM. BNP mRNA expression was increased fivefold (P < 0.001) after 48 h in culture without adrenergic stimulation. BNP mRNA expression was reduced (P < 0.0001) after stimulation with Iso while ANP expression remained similar to unstimulated cells. CGP prevented the Iso reduction in BNP mRNA. Iso stimulation at doses that reduced BNP mRNA expression increased TUNEL positive nuclei, an effect blocked by the beta1-antagonist CGP. In conclusion, we have demonstrated differential gene expression of ANP and BNP in AMCM in culture. Expression of BNP mRNA increases in AMCM in culture and beta1-adrenergic receptor stimulation attenuates increased BNP gene expression and results in apoptosis.


Asunto(s)
Factor Natriurético Atrial/metabolismo , Miocitos Cardíacos/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Antagonistas Adrenérgicos beta/farmacología , Animales , Factor Natriurético Atrial/fisiología , Células Cultivadas , Expresión Génica , Imidazoles/farmacología , Etiquetado Corte-Fin in Situ , Isoproterenol/farmacología , Ratones , Péptido Natriurético Encefálico , Proteínas del Tejido Nervioso/fisiología , Propanolaminas/farmacología , ARN Mensajero/metabolismo
2.
Basic Res Cardiol ; 97(3): 206-13, 2002 May.
Artículo en Inglés | MEDLINE | ID: mdl-12061390

RESUMEN

We tested the hypotheses that myocardial infarction in mice would lead to progressively worsening heart failure 12-18 weeks later and that exercise testing would provide a suitable means to evaluate left ventricular function sequentially. C57BL/6 mice (n = 69) underwent left coronary artery ligation (n = 50) or thoracotomy without ligation (n = 19). Sixteen animals (32%) died within 24 h of coronary ligation. Twenty additional animals (40%) died between days 3 and 14, and these mice showed infarct sizes of > 50% of the left ventricle. Fourteen animals (28%) that survived two weeks underwent echocardiography and treadmill testing 12 and 18 weeks after infarction, with no further mortality. Mice were then killed, morphometric assessment made, infarct size evaluated, and myocardial norepinephrine content and expression of BNP and ANF measured. Mice with infarcts >30% of the left ventricle (n = 6; 12% of original cohort) had left ventricular dilation (p < 0.0001) and hypertrophy (p < 0.001), impaired left ventricular systolic function (p < 0.0001) and reduced exercise duration (p = 0.03) and total work (p = 0.03) 12-18 weeks after infarction. Mice with infarcts <30% of the left ventricle (n = 8; 16% of original cohort) had no significant functional changes or left ventricular remodeling. Hearts from mice with infarcts > 30 % had reduced myocardial norepinephrine levels (MI <30%: 177+/-54 pg/mg, n = 6; MI >30%: 66+/-14 pg/mg wet weight, n = 4; p = 0.005) and increased mRNA content of BNP (p < 0.03) and ANF (p = 0.023). Coronary artery occlusion in mice provides a relevant model of clinical heart failure that is progressive and can be assessed by sequential exercise testing, providing a means to study the development of heart failure and its treatment.


Asunto(s)
Gasto Cardíaco Bajo/etiología , Infarto del Miocardio/complicaciones , Animales , Factor Natriurético Atrial/metabolismo , Gasto Cardíaco Bajo/diagnóstico por imagen , Progresión de la Enfermedad , Ecocardiografía , Masculino , Ratones , Ratones Endogámicos C57BL , Actividad Motora , Infarto del Miocardio/diagnóstico por imagen , Infarto del Miocardio/patología , Infarto del Miocardio/fisiopatología , Miocardio/metabolismo , Péptido Natriurético Encefálico , Norepinefrina/metabolismo
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