Changes in adrenomedullin and receptor activity-modifying protein 2 mRNA in myocardium and vessels during L-NNA-induced hypertension in rats / 生理学报
Acta Physiologica Sinica
; (6): 337-341, 2002.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-318989
Biblioteca responsável:
WPRO
ABSTRACT
To explore the changes in adrenomedullin (ADM) and receptor activity-modifying protein 2 (RAMP2) mRNA in myocardium and vessels in hypertension, a hypertensive rat model was prepared by administering L-NNA. Contents of ADM in plasma, myocardium and vessels were measured by radioimmunoassay (RIA). The levels of pro-ADM mRNA of myocardium and vessels were determined by competitive quantitative RT-PCR. The results showed that L-NNA induced hypertension and cardiomegaly. The ratio of heart to body weight increased by 35.5% (P<0.01). In hypertensive rats the ir-ADM in plasma, myocardium and vessels was increased by 80%, 72% and 57% (P<0.01), respectively compared with the control. The amounts of ADM mRNA in myocardium and vessels were increased by 50% and 109.2% (P<0.05), respectively, and the amounts of RAMP2 mRNA was increased by 132% and 87% (P<0.01), respectively, compared with control. The levels of ADM in myocardium and vessels were positively correlated with RAMP2 mRNA, the correlation coefficients were 0.741 and 0.885 (P<0.01), respectively. The results obtained indicate that in hypertensive rats, ADM is elevated in plasma, myocardium and ves-myocardium and vessel, and ADM and RAMP2 mRNA are up-regulated in myocardium and vessel. The ADM/RAMP2 system may play an important role in the pathogenesis of hypertension.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
RNA Mensageiro
/
Regulação para Cima
/
Cardiomegalia
/
Nitroarginina
/
Reação em Cadeia da Polimerase Via Transcriptase Reversa
/
Adrenomedulina
/
Proteína 2 Modificadora da Atividade de Receptores
/
Hipertensão
/
Metabolismo
Limite:
Animais
Idioma:
Chinês
Revista:
Acta Physiologica Sinica
Ano de publicação:
2002
Tipo de documento:
Artigo