Abstract 205: Differing Cardiac Phenotypes Between PP1α and PP1β Heart-Specific Gene-Deleted Mice

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Mannix Messier ◽  
Ruijie Liu ◽  
Jeffery Molkentin
Keyword(s):  
Weight Ratio ◽  
Pressure Overload ◽  
Cardiac Contraction ◽  
Calcium Handling ◽  
Heart Weight ◽  
Specific Gene ◽  
Mouse Heart ◽  
Major Protein ◽  
Intron 1 ◽  
Mammalian Tissues

Background: Protein phosphatase 1 is the major protein serine/threonine phosphatase in nearly all mammalian tissues, where it consists of three isoforms PP1α, PP1β, and PP1γ. However, the redundant or specific roles of each isoform in the heart is not known Methods: Each PP1 isoform was conditionally deleted in the mouse heart using a Cre-loxP approach. LoxP sites were introduced into intron 1 and 3 of each PP1α and PP1β. Both loxP-targeted lines were bred with mice expressing β-myosin heavy chain promoter driven Cre to achieve isoform specific gene deletion in the heart. Echocardiography was performed in these mice at different ages. We also investigated protein phosphorylation status of selected PP1 targets that underlie cardiac contraction and calcium handling from the hearts of these deleted mice. Results: Heart-specific deletion of PP1α caused a reduction of fractional shortening and worsening of cardiac function. Two weeks after transaortic constriction (TAC), PP1α deleted mice had greater increases in heart-weight to body-weight ratio compared with control mice, suggesting that PP1α was important for proper cardiac compensation. Interestingly, however, combined deletion of both PP1α and PP1β rescued the cardiac performance defects observed in PP1α deleted mice. Mechanistically, we found that deletion of PP1αβ led to increased phospholamban serine 16 and threonine 17 phosphorylation compared to that of PP1α. In conclusion, we showed that PP1 isoforms play distinct roles in the heart in regulating contractility and compensation after pressure overload stimulation.

Abstract P112: Estradiol Induces Physiological Hypertrophic Growth in the Healthy Mouse Heart

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Georgios Kararigas ◽  
Ba Tiep Nguyen ◽  
Hubertus Jarry ◽  
Vera Regitz-Zagrosek
Keyword(s):  
Weight Ratio ◽  
Treated Group ◽  
Left Ventricular ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Mouse Heart ◽  
Cross Sectional ◽  
Hypertrophic Growth ◽  
Protein Levels ◽  
Cycle Regulation

Estradiol-17beta (E2) has been shown to exert anti-hypertrophic actions by either attenuating or blunting the development of left ventricular hypertrophy. However, the vast majority of these studies have been performed in stressed or diseased hearts. Consequently, very little is known about the actions of E2 in the stress- and disease-free heart. The aim of our study was to identify and characterize structurally and molecularly the role of E2 in the healthy heart. Female C57Bl/6J mice were ovariectomized at the age of two months. Mice were randomly assigned into groups feeding on either an E2-containing (n = 19) or soy-free (Ctrl; n = 19) diet for three months. Following this, all mice were sacrificed and hearts were collected for weight measurement. Left ventricles were analyzed structurally by immunohistochemistry and molecularly by genome-wide expression profiling. E2 led to an increase in the heart weight (11%; P < 0.001) and the heart-to-body weight ratio (32%; P < 0.001) compared to Ctrl mice. Cardiomyocyte cross-sectional area revealed cardiomyocyte hypertrophy in E2 (n = 6) compared to Ctrl (n = 5) mice (32%; P = 0.004). Analysis of the left ventricular transcriptome identified 1059 probe sets (adjusted P ≤ 0.05) differentially expressed between E2 (n = 5) and Ctrl (n = 5). Hypergeometric testing for Gene Ontology showed most genes to be associated with cell cycle, regulation of growth, cell and tissue development. Pathway analysis revealed 140 pathways (adjusted P = 0.05) modulated between the two groups, such as the DNA replication and Wnt signaling pathways. Next, we tested the hypothesis that this hypertrophic effect of E2 is of the physiological type. To this extent, we identified that angiogenesis was increased with cardiac growth as determined by the microarray analysis and VEGF-A protein levels assessed by Western blotting. Furthermore, the embryonic gene program was not activated and no fibrosis was observed in the E2-treated group. In conclusion, our study is the first to demonstrate pro-hypertrophic actions of E2 in the healthy heart through the modulation of growth-related genes and pathways. Due to that we have characterized the hypertrophic effect of E2 as physiological, we expect this effect to be beneficial for the heart.

scholarly journals Impacts of a Specific Cyclooxygenase-2 Inhibitor on Pressure Overload–Induced Myocardial Hypertrophy in Rats

2019 ◽  
Vol 22 (6) ◽  
pp. E432-E437
Author(s):  
Zhixiang Xie ◽  
Shuyin Wang ◽  
Zijing Liang ◽  
Liangbo Zeng ◽  
Rongde Lai ◽  
...  
Keyword(s):  
Myocardial Hypertrophy ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cyclooxygenase 2 ◽  
Inflammatory Factors ◽  
Heart Weight ◽  
Sham Operation ◽  
Surgery Group ◽  
Tnf Α

Objective: The aim of this study was to observe the impacts of the specific cyclooxygenase-2 inhibitor celecoxib on cardiac structures, functions, and inflammatory factors during the process of pressure overload–induced myocardial hypertrophy. Methods: Twenty-four male Sprague Dawley rats were randomly divided into 3 groups: the sham operation group, the surgery group, and the celecoxib group. The model was established according to the abdominal aortic coarctation method. Results: At 16 weeks, rats in the celecoxib group were fed a celecoxib-mixed diet (10 mg/kg) for 8 consecutive weeks. At week 24 after model establishment, the cardiac structures and functions were observed; changes in the levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, prostaglandin E2 (PGE2), C-reactive protein (CRP), and uric acid (UA) were detected; and the contents of Smad1/2/3 proteins (Smad1, Smad2, and Smad3)  were determined. Left ventricular mass index, the heart weight/body weight ratio, and TNF-α, TGF-β, PGE2, CRP, and UA levels of the celecoxib group were all significantly decreased relative to those of the surgery group (P < .05); moreover, the cardiac functions were significantly improved compared to those of the surgery group (P < .05). Conclusions: These results show that inflammatory factors are involved in the myocardial hypertrophy process and that celecoxib may reverse myocardial hypertrophy through a variety of pathways.

Sarcoplasmic reticulum-related changes in cytosolic calcium in pressure-overload-induced feline LV hypertrophy

1993 ◽  
Vol 265 (6) ◽  
pp. H2009-H2016 ◽  
Author(s):  
B. A. Bailey ◽  
S. R. Houser
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Time Course ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Cytosolic Calcium ◽  
Left Ventricular ◽  
Heart Weight ◽  
Body Weight Ratio ◽  
Rest Periods ◽  
Premature Beats

Alterations in Ca2+ homeostasis that involve the sarcoplasmic reticulum (SR) were studied in feline left ventricular (LV) myocytes isolated from hearts with LV hypertrophy induced by slow, progressive pressure overload. At death, severe hypertrophy was evidenced by increased heart weight-to-body weight ratio (8.4 +/- 0.6 vs. 4.2 +/- 0.2 g/kg in controls). Steady-state Ca2+ transients (measured as. indo 1 fluorescence at 410 nm/480 nm; I410/I480) in LV hypertrophy (LVH) myocytes had diminished peak amplitudes (I410/I480 2.28 +/- 0.07 vs. 2.53 +/- 0.07 in controls) and prolonged durations (0.75 +/- 0.03 vs. 0.59 +/- 0.02 s in controls). The magnitude of shortening was reduced and the contractile duration was prolonged in LVH myocytes. The idea that changes in SR function are responsible for these alterations in the Ca2+ transient was tested by studying two aspects of SR-related Ca2+ homeostasis. Restitution of releasable SR Ca2+ was studied by measuring indo 1 transients and contractions during premature beats. The time course of restitution of both the indo 1 transient and contraction of hypertrophy myocytes was significantly slower than in controls. These data suggest that restitution of releasable SR Ca2+ is slowed in hypertrophy myocytes. The reduction of the indo 1 transient and contraction in beats following long rest periods (rest decay) was measured to determine the rate of Ca2+ loss from the SR. Rest decay was significantly (P < 0.05) more pronounced in hypertrophy myocytes, suggesting that Ca2+ loss from the SR is accelerated in these myocytes. (ABSTRACT TRUNCATED AT 250 WORDS)

Abstract 341: Both Beta-1 and Beta-2 Adrenergic Receptors (ARs) are Required for Pressure Overload Cardiac Hypertrophy

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Mingming Zhao ◽  
Roger Wagner ◽  
Giovanni Fajardo ◽  
Takashi Urashima ◽  
Sara Farahani ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Kinase Inhibitor ◽  
Binding Protein ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Heart Weight ◽  
Lv Function ◽  
List Type ◽  
Hypertrophic Response ◽  
Calgranulin B

In isolated myocytes, hypertrophy induced by norepinephrine is mediated via β-ARs, however, in vivo, mice with deletions of both major cardiac β-ARs still develop hypertrophy with pressure overload. The mechanism by which the heart adapts to pressure overload, producing either adaptive or maladaptive remodeling is still not completely understood. To study the role of β-ARs in pressure overload hypertrophy, we performed transverse aortic constriction (TAC) in congenic mice with targeted deletions of β1, β2 and both β1 and β2-ARs and in sham controls. After 3 wks, β1−/− mice showed a 21% increase in heart weight to body weight ratio (HW/BW) vs. sham, similar to WT (HW/BW 5.02 ± 0.72 for β1−/− vs. 5.20 ± 0.92 for WT). β2−/− mice showed an exaggerated (49%) hypertrophic response (HW/BW 5.81 ± 0.53, p < 0.001 vs. WT). Only when both β-ARs were ablated was hypertrophy fully attenuated: in β1β2−/− mice HW/BW increased only 8% (HW/BW 4.30 ± 0.31, p < 0.01 vs. WT). Echocardiography showed that peak band gradient was not different between groups (WT 45.3 ± 4.1, β1−/− 47.2 ± 10.2, β2−/− 49.0 ± 9.7, β1β2−/− 53.2 ± 11.3 mmHg) and all groups maintained normal LV function. Morphometric analysis confirmed the absence of hypertrophy in the β1β2−/−: mean cross-sectional area for WT was 254.7 ± 34.9 vs. β1β2−/− 115.8 ± 16.7μm 2 , which was not different from sham. Gene microarray analysis detected a set of genes which were differentially expressed in β1β2−/− vs. WT, β1−/−, or β2−/−: S100 calcium binding protein A9/calgranulin B (S100a9, 4.5-fold up); Cyclin-dependent kinase inhibitor 1A/P21 (Cdkn1a, 3.8-fold up); Metallothioneins Mt1 (3-fold up) and Mt2 (2.7-fold up); FK506 binding protein 5, a glucocorticoid receptor-regulating co-chaperone and calcineurin inhibitor (3.2-fold up). In contrast, TGFβ2 was upregulated in WT, β1−/− and β2−/− but not in β1β2−/−. Differentially regulated genes were validated by SYBR QRT-PCR on the same RNA samples. Thus, β2-AR signaling may serve to limit the hypertrophic response to pressure afterload. However, both β-ARs are required for the development of a normal hypertrophic response. Ablation of both β-AR subtypes alters expression of several genes, some of which may be critical to the hypertrophic program.

Transgenic upregulation ofIK1in the mouse heart leads to multiple abnormalities of cardiac excitability

2004 ◽  
Vol 287 (6) ◽  
pp. H2790-H2802 ◽  
Author(s):  
Jingdong Li ◽  
Meredith McLerie ◽  
Anatoli N. Lopatin
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Weight Ratio ◽  
Monophasic Action Potential ◽  
Heart Weight ◽  
Slow Phase ◽  
Mouse Heart ◽  
Premature Ventricular Contractions ◽  
Surface Ecg ◽  
Cardiac Excitability

To assess the functional significance of upregulation of the cardiac current ( IK1), we have produced and characterized the first transgenic (TG) mouse model of IK1upregulation. To increase IK1density, a pore-forming subunit of the Kir2.1 (green fluorescent protein-tagged) channel was expressed in the heart under control of the α-myosin heavy chain promoter. Two lines of TG animals were established with a high level of TG expression in all major parts of the heart: line 1 mice were characterized by 14% heart hypertrophy and a normal life span; line 2 mice displayed an increased mortality rate, and in mice ≤1 mo old, heart weight-to-body weight ratio was increased by >100%. In adult ventricular myocytes expressing the Kir2.1-GFP subunit, IK1conductance at the reversal potential was increased ∼9- and ∼10-fold in lines 1 and 2, respectively. Expression of the Kir2.1 transgene in line 2 ventricular myocytes was heterogeneous when assayed by single-cell analysis of GFP fluorescence. Surface ECG recordings in line 2 mice revealed numerous abnormalities of excitability, including slowed heart rate, premature ventricular contractions, atrioventricular block, and atrial fibrillation. Line 1 mice displayed a less severe phenotype. In both TG lines, action potential duration at 90% repolarization and monophasic action potential at 75–90% repolarization were significantly reduced, leading to neuronlike action potentials, and the slow phase of the T wave was abolished, leading to a short Q-T interval. This study provides a new TG model of IK1upregulation, confirms the significant role of IK1in cardiac excitability, and is consistent with adverse effects of IK1upregulation on cardiac electrical activity.

Abstract 208: Parkin Contributes to the Development of Cardiac Hypertrophy in Response to Cardiac Pressure Overload

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Sarah E Shires ◽  
Dieter A Kubli ◽  
Eileen R Gonzalez ◽  
Nicole H Purcell ◽  
Åsa B Gustafsson
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Expression Profiles ◽  
Rapid Development ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Heart Weight ◽  
Loss Of Function ◽  
Functional Importance ◽  
Knock Out

Parkin is an E3 ubiquitin ligase known to mediate mitochondrial clearance by marking damaged mitochondria for autophagy. Our lab has previously shown that Parkin is important for stress adaptation following myocardial infarction, and that loss of Parkin leads to accumulation of dysfunctional mitochondria. However, whether Parkin plays a role in cardiac adaptation to pressure overload is currently unknown. Here we investigated the functional importance of Parkin in cardiac hypertrophy and development of heart failure in response to hemodynamic stress. Wild type (WT), Parkin knock out (Parkin -/- ), and cardiac-specific Parkin transgenic (Parkin-TG) mice were subjected to trans-aortic constriction (TAC). Cardiac anatomy and function was evaluated by histology and echocardiography. Inflammation and hypertrophy gene expression profiles were assessed using qPCR and immunohistochemistry. We discovered that after 2 weeks of TAC, cardiac hypertrophy markers were not increased in hearts from Parkin -/- mice, and there was no increase in the heart weight to body weight ratio (HW/BW). However, after 8 weeks of TAC, Parkin -/- mice showed similar cardiac hypertrophy and loss of function as WT hearts. Parkin deficient hearts also displayed increased interstitial and perivascular fibrosis compared to WT hearts after 8 weeks of TAC. This suggests that there is a delay in activating the hypertrophy program in the absence of Parkin, and that lack of Parkin leads to excessive fibrosis. In contrast, Parkin-TG mice showed a rapid development of hypertrophy and progression to heart failure compared to WT mice. Interestingly, we observed no differences in either mitochondrial content or LC3 levels after two weeks of TAC in Parkin-TG hearts, suggesting that the rapid development of hypertrophy and early progression to heart failure was not due to excessive mitophagy. These data suggest that Parkin plays an important role in the activation of the cardiac hypertrophy program and that this function may be independent of its role in regulating mitophagy. Thus, this study provides novel insight into the functional importance of Parkin in the heart. Additional studies are needed to determine the mechanism of how Parkin regulates cardiac hypertrophy.

Overexpression of FGF-2 increases cardiac myocyte viability after injury in isolated mouse hearts

2001 ◽  
Vol 280 (3) ◽  
pp. H1039-H1050 ◽  
Author(s):  
Farah Sheikh ◽  
David P. Sontag ◽  
Robert R. Fandrich ◽  
Elissavet Kardami ◽  
Peter A. Cattini
Keyword(s):  
Cardiac Myocyte ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Weight Ratio ◽  
Capillary Density ◽  
Cardiac Differentiation ◽  
Heart Weight ◽  
Mouse Heart ◽  
Differentiation Markers ◽  
Fgf Receptor

We generated transgenic (TG) mice overexpressing fibroblast growth factor (FGF)-2 protein (22- to 34-fold) in the heart. Chronic FGF-2 overexpression revealed no significant effect on heart weight-to-body weight ratio or expression of cardiac differentiation markers. There was, however, a significant 20% increase in capillary density. Although there was no change in FGF receptor-1 expression, relative levels of phosphorylated c-Jun NH2-terminal kinase and p38 kinase as well as of membrane-associated protein kinase C (PKC)-α and total PKC-ε were increased in FGF-2-TG mouse hearts. An isolated mouse heart model of ischemia-reperfusion injury was used to assess the potential of increased endogenous FGF-2 for cardioprotection. A significant 34–45% increase in myocyte viability, reflected in a decrease in lactate dehydrogenase released into the perfusate, was observed in FGF-2 overexpressing mice and non-TG mice treated exogenously with FGF-2. In conclusion, FGF-2 overexpression causes augmentation of signal transduction pathways and increased resistance to ischemic injury. Thus, stimulation of endogenous FGF-2 expression offers a potential mechanism to enhance cardioprotection.

Estrogen receptor-β mediates male-female differences in the development of pressure overload hypertrophy

2005 ◽  
Vol 288 (2) ◽  
pp. H469-H476 ◽  
Author(s):  
Maryanne Skavdahl ◽  
Charles Steenbergen ◽  
James Clark ◽  
Page Myers ◽  
Tracy Demianenko ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Estrogen Receptor Α ◽  
Epidemiological Studies ◽  
Estrogen Receptor Β ◽  
Heart Weight ◽  
Receptor Subtypes ◽  
Lung Weight

The goal of this study was to determine the role of estrogen receptor subtypes in the development of pressure overload hypertrophy in mice. Epidemiological studies have suggested gender differences in the development of hypertrophy and heart disease, but the mechanism and the role of estrogen receptor subtypes are not established. We performed transverse aortic constriction (TAC) and sham operations in male and female wild-type (WT) mice and mice lacking functional estrogen receptor-α [α-estrogen receptor knockout (α-ERKO)] and mice lacking estrogen receptor-β (β-ERKO). Body, heart, and lung weights were measured 2 wk postsurgery. WT male mice subjected to TAC showed a 64% increase in the heart weight-to-body weight ratio (HW/BW) compared with sham, and WT males have increased lung weight at 2 wk. WT female mice subjected to TAC showed a 31% increase in HW/BW compared with sham, which was significantly less than their male counterparts and with no evidence of heart failure. α-ERKO females developed HW/BW nearly identical to that seen in WT littermate females in response to TAC, indicating that estrogen receptor-α is not essential for the attenuation of hypertrophy observed in WT females. In contrast, β-ERKO females responded to TAC with a significantly greater increase in HW/BW than WT littermate females. β-ERKO females have lower expression of lipoprotein lipase at baseline than WT or α-ERKO females. These data suggest an important role for estrogen receptor-β in attenuating the hypertrophic response to pressure overload in females.

Cardiac myocyte volume, Ca2+ fluxes, and sarcoplasmic reticulum loading in pressure-overload hypertrophy

1997 ◽  
Vol 272 (5) ◽  
pp. H2425-H2435 ◽  
Author(s):  
L. M. Delbridge ◽  
H. Satoh ◽  
W. Yuan ◽  
J. W. Bassani ◽  
M. Qi ◽  
...  
Keyword(s):  
Steady State ◽  
Sarcoplasmic Reticulum ◽  
Laser Scanning ◽  
Cardiac Myocyte ◽  
Membrane Surface ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Heart Weight ◽  
The Relationship

Alterations in cellular Ca2+ transport and excitation-contraction coupling may contribute to dysfunction in cardiac hypertrophy. Left ventricular myocytes were isolated from rat hearts after 15-18 wk of suprarenal abdominal aortic banding to evaluate the hypothesis that hypertrophy alters the relationship between Ca2+ current (ICa) and sarcoplasmic reticulum (SR) Ca2+ load during steady-state voltage-clamp depolarization. Mean arterial pressure (MAP) and heart weight-to-body weight ratio of banded (B) animals were significantly higher than in control or sham-operated animals (C). Isolated myocyte dimensions and volume increased in parallel with whole heart hypertrophy and elevation in MAP. However, the relationship between membrane surface area (measured by capacitance) and cell volume (measured by laser scanning confocal microscopy) was unaltered (C: 8.9 +/- 0.3; B: 8.5 +/- 0.4 pF/pl). No differences in the voltage dependence of ICa activation, steady-state inactivation, or recovery from inactivation were detected between C and B myocytes. Maximal ICa density for the two groups was also not different either under basal conditions (C: 4.28 +/- 0.98; B: 4.57 +/- 0.60 pA/pF) or in the presence of 1 microM isoproterenol (C: 16.6 +/- 2.3; B: 16.5 +/- 2.3 pA/pF). The fraction of Ca2+ released from the SR by a single twitch was 55.4 +/- 9.4% in C and 37.1 +/- 6.9% in B (not significantly different). Steady-state Ca2+ influx during a twitch was calculated in units of micromoles per liter of nonmitochondrial volume from the integral of ICa (C: 13.4 +/- 0.7 microM; B: 13.3 +/- 0.8 microM). The SR Ca2+ load was similarly calculated by integration of Na+/Ca2+ exchange current induced by rapid caffeine application (C: 140 +/- 9 microM; B: 169 +/- 18 microM). We conclude that significant cellular hypertrophy is associated with proportional increases in sarcolemmal ICa influx, SR Ca2+ loading, and the amount of SR Ca2+ released in this model of pressure overload.

ANG II receptor blockade prevents ventricular hypertrophy and ANF gene expression with pressure overload in mice

1994 ◽  
Vol 266 (6) ◽  
pp. H2468-H2475 ◽  
Author(s):  
H. A. Rockman ◽  
S. P. Wachhorst ◽  
L. Mao ◽  
J. Ross
Keyword(s):  
Body Weight ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Systolic Pressure ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Heart Weight ◽  
Receptor Blockade ◽  
Body Weight Ratio

There is increasing evidence that the renin-angiotensin system may play a important role in cardiac hypertrophy. To assess the role of angiotensin II in the induction of cardiac hypertrophy, three groups of adult mice were subjected to left ventricular pressure overload by transverse aortic constriction (TAC). For the next 7 days the groups received either the specific angiotensin II subtype 1 receptor (AT1) antagonist (losartan, 1.05 g/l; n = 17), an angiotensin enzyme inhibitor (captopril, 2 g/l; n = 17), or no treatment (n = 22) administered in the drinking water and compared with three similarly treated sham-operated groups (n = 7 each). TAC resulted in a significant increase in heart weight-to-body weight ratio (0.634 +/- 0.087 vs. 0.525 +/- 0.039, g/g x 100, P < 0.05), which was prevented by losartan (0.506 +/- 0.069, g/g x 100, P < 0.0001) despite similar hemodynamic load (proximal systolic pressure 146 +/- 31 vs. 136 +/- 32 mmHg, untreated vs. losartan, P = NS). Proximal systolic pressure was positively correlated with the development of ventricular hypertrophy. In the presence of AT1-receptor blockade, the increase in heart weight-to-body weight ratio at any given systolic pressure was significantly attenuated compared with untreated TAC mice. The increase in heart weight-to-body weight ratio was also significantly attenuated by captopril compared with untreated banded controls (0.542 +/- 0.091, g/g x 100, P = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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