TY - JOUR
T1 - Angiotensin II receptor gene expression in hypertrophied left ventricles of rat hearts
AU - Wolf, Konrad
AU - Della Bruna, Roberto
AU - Bruckschlegel, Günther
AU - Schunkert, Heribert
AU - Riegger, Günter A.J.
AU - Kurtz, Armin
PY - 1996
Y1 - 1996
N2 - Objective. To examine the expression of angiotensin II AT(1a), AT(1b) and AT2 receptor genes in the left ventricles of rats subjected to ventricular pressure overloading induced by aortic banding for 6 weeks and then 6 weeks medical treatment. Results. Aortic banding was related to an increase in relative weight of the left ventricle from 1.73 ± 0.06 (sham-operated) to 2.81 ± 0.25 g/kg, an increase in β-myosin:α-myosin messenger RNA (mRNA) ratio from 0.30 ± 0.02 to 1.94 ± 0.55 and an 18-fold increase in left ventricular atrial natriuretic peptide mRNA levels. In contrast, left ventricular pressure overload hypertrophy was not related to a significant change in the abundance of AT(1a) and AT(1b) mRNA, which were expressed in a relative ratio of 5:1. Similarly, the abundance of AT2 mRNA was not significantly changed in hypertrophied ventricles. In rats receiving the angiotensin II AT1 receptor antagonist losartan (40 mg/kg) for 6 weeks after banding, relative heart weights were β-myosin:α-myosin ratio was natriuretic peptide mRNA levels displayed a blunted increase (11-fold over sham-treated controls), documenting a significant amelioration of left ventricular hypertrophy by blockade of the AT1 receptor. Conclusion. Losartan treatment in parallel did not affect AT(1A), AT(1b) and AT2 receptor mRNA levels, which were not different from those in vehicle-treated or sham-treated controls. These findings confirm that left ventricular hypertrophy in the rat is associated with increased ventricular expression of β-myosin and of atrial natriuretic peptide and with reduced expression of α-myosin. Despite these significant changes in cardiac gene expression no alteration was observed in AT(1A), AT(1b) and AT2 receptor mRNA levels.
AB - Objective. To examine the expression of angiotensin II AT(1a), AT(1b) and AT2 receptor genes in the left ventricles of rats subjected to ventricular pressure overloading induced by aortic banding for 6 weeks and then 6 weeks medical treatment. Results. Aortic banding was related to an increase in relative weight of the left ventricle from 1.73 ± 0.06 (sham-operated) to 2.81 ± 0.25 g/kg, an increase in β-myosin:α-myosin messenger RNA (mRNA) ratio from 0.30 ± 0.02 to 1.94 ± 0.55 and an 18-fold increase in left ventricular atrial natriuretic peptide mRNA levels. In contrast, left ventricular pressure overload hypertrophy was not related to a significant change in the abundance of AT(1a) and AT(1b) mRNA, which were expressed in a relative ratio of 5:1. Similarly, the abundance of AT2 mRNA was not significantly changed in hypertrophied ventricles. In rats receiving the angiotensin II AT1 receptor antagonist losartan (40 mg/kg) for 6 weeks after banding, relative heart weights were β-myosin:α-myosin ratio was natriuretic peptide mRNA levels displayed a blunted increase (11-fold over sham-treated controls), documenting a significant amelioration of left ventricular hypertrophy by blockade of the AT1 receptor. Conclusion. Losartan treatment in parallel did not affect AT(1A), AT(1b) and AT2 receptor mRNA levels, which were not different from those in vehicle-treated or sham-treated controls. These findings confirm that left ventricular hypertrophy in the rat is associated with increased ventricular expression of β-myosin and of atrial natriuretic peptide and with reduced expression of α-myosin. Despite these significant changes in cardiac gene expression no alteration was observed in AT(1A), AT(1b) and AT2 receptor mRNA levels.
KW - Angiotensin II receptors
KW - Atrial natriuretic peptide
KW - Hypertrophy
KW - Losartan
KW - α-myosin/β-myosin
UR - http://www.scopus.com/inward/record.url?scp=0029873234&partnerID=8YFLogxK
U2 - 10.1097/00004872-199603000-00012
DO - 10.1097/00004872-199603000-00012
M3 - Article
C2 - 8723989
AN - SCOPUS:0029873234
SN - 0263-6352
VL - 14
SP - 349
EP - 354
JO - Journal of Hypertension
JF - Journal of Hypertension
IS - 3
ER -