In situ mitochondrial function in volume overload- and pressure overload-induced cardiac hypertrophy in rats

1995 ◽  
Vol 90 (4) ◽  
pp. 305-313 ◽  
Author(s):  
Mong Hung Bui ◽  
R. Janati-Idrissi ◽  
B. Besson ◽  
M. Laplace
Keyword(s):  
Cardiac Hypertrophy ◽  
Mitochondrial Function ◽  
Pressure Overload ◽  
Volume Overload

Collagen characterization in volume-overload- and pressure-overload-induced cardiac hypertrophy in minipigs

1993 ◽  
Vol 265 (2) ◽  
pp. H434-H438 ◽  
Author(s):  
J. Harper ◽  
E. Harper ◽  
J. W. Covell
Keyword(s):  
Cardiac Hypertrophy ◽  
Porcine Model ◽  
Pressure Overload ◽  
Volume Overload ◽  
Heart Tissue ◽  
Canine Heart ◽  
Cross Link ◽  
Collagen Types ◽  
Collagen Concentration ◽  
Pepsin Digestion

Previous studies in several different species have shown reduced extractability of collagens in some types of cardiac hypertrophy (volume overload) but not others (pressure overload). The objective of the present study was to examine collagen proteins from the same species (minipigs) with both pressure-overload- and volume-overload-induced cardiac hypertrophy. Hypertrophy was induced by two methods: thoracic banding of the aorta to create pressure overload and arteriovenous shunt to cause volume overload in a porcine model. Collagen types I, III, IV, and V were isolated by pepsin digestion from normal and hypertrophied pig left ventricle tissues. Types I and III collagens from normal and hypertrophied samples, when separated from types IV and V, were digested with cyanogen bromide (CB), and the peptides were examined. Collagen concentration was increased in myocardium removed from hearts subjected to volume overload and unchanged in hearts subjected to pressure overload. The extractability of total collagen was unaffected in pressure-overloaded left ventricles but lower in samples from volume-overloaded hearts. CB digestion cleaved all of the types I and III collagens into similar smaller CB peptides with the exception of a 100-kDa peptide that was observed in both control and hypertrophied hearts. This peptide corresponds to one of the high-molecular-weight peptides found in canine heart tissue. The mature collagen cross-link hydroxylysylpyridinoline (HP) was identified in normal and hypertrophied types I and III collagen from porcine sources. Pressure-overload- and volume-overload-induced cardiac hypertrophy in the pig produced different alterations in the extracellular matrix.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Early sequence of cardiac adaptations and growth factor formation in pressure- and volume-overload hypertrophy

2000 ◽  
Vol 279 (3) ◽  
pp. H976-H985 ◽  
Author(s):  
Pietro Amedeo Modesti ◽  
Simone Vanni ◽  
Iacopo Bertolozzi ◽  
Ilaria Cecioni ◽  
Gianluca Polidori ◽  
...  
Keyword(s):  
Growth Factor ◽  
Myocardial Contractility ◽  
Pressure Overload ◽  
Volume Overload ◽  
Aortic Banding ◽  
Peptide Formation ◽  
Cardiac Adaptation ◽  
Igf I ◽  
Hemodynamic Measurements

To investigate the time sequence of cardiac growth factor formation, echocardiographic and hemodynamic measurements were performed at scheduled times, and mRNAs for angiotensinogen, prepro-endothelin-1 (ppET-1), and insulin-like growth factor I (IGF-I) were quantified with RT-PCR and localized with in situ hybridization in pigs (fluothane anesthesia) by use of pressure or volume overload (aortic banding and aorta-cava fistula, respectively). Relative peptide formation was also measured by radioimmunoassay. In pressure overload, angiotensinogen and ppET-1 mRNA overexpression on myocytes (13 times vs. sham at 3 h and 112 times at 6 h, respectively) was followed by recovery (12 h) of initially decreased (0.5–6 h) myocardial contractility. In volume overload, contractility was not decreased, the angiotensinogen gene was slightly upregulated at 6 h (6.7 times), and ppET-1 was not overexpressed. IGF-I mRNA was overexpressed on myocytes (at 24 h) in both volume and pressure overload (14 times and 37 times, respectively). In the latter setting, a second ppET-1 overexpression was detectable on myocytes at 7 days. In conclusion, acute cardiac adaptation responses involve different growth factor activation over time in pressure versus volume overload; growth factors initially support myocardial contractility and thereafter induce myocardial hypertrophy.

Humoral factor(s) produced by pressure overload enhance cardiac hypertrophy and natriuretic peptide expression

1997 ◽  
Vol 273 (1) ◽  
pp. H113-H118 ◽  
Author(s):  
T. Iso ◽  
M. Arai ◽  
A. Wada ◽  
K. Kogure ◽  
T. Suzuki ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Aortic Coarctation ◽  
Pressure Overload ◽  
Humoral Factor ◽  
Myosin Isoforms ◽  
Hypertrophic Response ◽  
Cardiac Atrophy ◽  
Transplanted Hearts

Chronic pressure overload is known to increase cardiac mass and expression levels of both atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNAs. Although mechanical stretching of cardiac myocytes could cause these changes, humoral factor(s) secondary to pressure overload may also be involved. To dissociate humoral effects from the effects of mechanical loading on cardiac hypertrophic responses, we examined expression of ANP and BNP at both mRNA and protein levels and proportions of myosin isoforms in transplanted cervical hearts that were mechanically unloaded under conditions with or without hypertension by aortic coarctation. Seven days after transplantation, cardiac atrophy that usually occurs in transplanted hearts without hypertension by coarctation was prevented in the transplanted hearts with hypertension by coarctation. The levels of expression of ANP and BNP mRNAs were increased in the transplanted hearts with relative to those without hypertension by coarctation. The plasma level of angiotensin II was higher in rats with than without hypertension by coarctation. Plasma endothelin-1 levels were not significantly different between the two groups. In addition, levels of expression of ANP and BNP mRNAs were increased in the transplanted hearts without hypertension relative to those in the in situ hearts. The proportion of the V3 myosin isoform was also increased in the transplanted hearts without hypertension relative to the in situ hearts. These results indicate that humoral factor(s) secondary to the pressure overload produced by aortic coarctation enhanced the cardiac hypertrophic response and elevated the levels of mRNAs encoding these embryonic markers. Moreover, our findings regarding ANP and BNP expression in the transplanted hearts provide additional evidence that the fetal genes are reexpressed during the process of cardiac atrophy as well as in cardiac hypertrophy.

Myocardial capillary diffusion capacity in rat hearts with cardiac hypertrophy due to pressure and volume overload

1993 ◽  
Vol 265 (1) ◽  
pp. H61-H68 ◽  
Author(s):  
H. Wahlander ◽  
B. Haraldsson ◽  
P. Friberg
Keyword(s):  
Cardiac Hypertrophy ◽  
Vascular Resistance ◽  
Renal Hypertension ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Functional Adaptation ◽  
Arterial Stenosis ◽  
Coronary Vascular Resistance ◽  
Diffusion Capacity

The functional adaptation of the myocardial capillary bed in response to cardiac hypertrophy was studied in one volume overload (aortocaval fistula, ACF) and in one pressure overload model [left renal arterial stenosis, two-kidney, one-clip (2K,1C)]. Furthermore, a group where renal hypertension was reversed 1 wk before experimentation (UC-2K,1C) and a sham-operated (Sham) group were studied. Functional estimations of myocardial capillary diffusion capacity in terms of permeability surface area products (PS) per 100 g of myocardium were obtained by the single-injection indicator dilution technique in a Langendorff preparation. After 4 wk, ACF hearts, with 72% hypertrophy and normal minimal coronary vascular resistance (CVR), displayed an unchanged diffusion capacity, i.e., PS for Cr-EDTA and vitamin B12. This indicates a structural out-growth of the coronary vascular bed to match the increased demand of the tissue. 2K,1C hearts with marked elevations of minimal coronary vascular resistance and left ventricular hypertrophy (65%) showed higher PS values than Sham, implying that diffusion capacity was enhanced despite structural coronary vascular changes. These changes were completely reversed in UC-2K,1C. Thus the present data imply that myocardial capillary diffusion capacity was well maintained in volume overloaded cardiac hypertrophy and in contrast with earlier morphometric estimations, even enhanced in pressure overload hypertrophy.

scholarly journals NADPH oxidase-4 promotes eccentric cardiac hypertrophy in response to volume overload

2019 ◽  
Author(s):  
Moritz Schnelle ◽  
Iain Sawyer ◽  
Narayana Anilkumar ◽  
Belal A Mohamed ◽  
Daniel A Richards ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Cardiac Hypertrophy ◽  
Interstitial Fibrosis ◽  
Pressure Overload ◽  
Volume Overload ◽  
Capillary Density ◽  
Left Ventricular ◽  
Cardiac Cells ◽  
Cross Sectional ◽  
Nadph Oxidase 4

Abstract Aims Chronic pressure or volume overload induce concentric vs. eccentric left ventricular (LV) remodelling, respectively. Previous studies suggest that distinct signalling pathways are involved in these responses. NADPH oxidase-4 (Nox4) is a reactive oxygen species-generating enzyme that can limit detrimental cardiac remodelling in response to pressure overload. This study aimed to assess its role in volume overload-induced remodelling. Methods and results We compared the responses to creation of an aortocaval fistula (Shunt) to induce volume overload in Nox4-null mice (Nox4−/−) vs. wild-type (WT) littermates. Induction of Shunt resulted in a significant increase in cardiac Nox4 mRNA and protein levels in WT mice as compared to Sham controls. Nox4−/− mice developed less eccentric LV remodelling than WT mice (echocardiographic relative wall thickness: 0.30 vs. 0.27, P < 0.05), with less LV hypertrophy at organ level (increase in LV weight/tibia length ratio of 25% vs. 43%, P < 0.01) and cellular level (cardiomyocyte cross-sectional area: 323 µm2 vs. 379 μm2, P < 0.01). LV ejection fraction, foetal gene expression, interstitial fibrosis, myocardial capillary density, and levels of myocyte apoptosis after Shunt were similar in the two genotypes. Myocardial phospho-Akt levels were increased after induction of Shunt in WT mice, whereas levels decreased in Nox4−/− mice (+29% vs. −21%, P < 0.05), associated with a higher level of phosphorylation of the S6 ribosomal protein (S6) and the eIF4E-binding protein 1 (4E-BP1) in WT compared to Nox4−/− mice. We identified that Akt activation in cardiac cells is augmented by Nox4 via a Src kinase-dependent inactivation of protein phosphatase 2A. Conclusion Endogenous Nox4 is required for the full development of eccentric cardiac hypertrophy and remodelling during chronic volume overload. Nox4-dependent activation of Akt and its downstream targets S6 and 4E-BP1 may be involved in this effect.

scholarly journals Cardiac Natriuretic Peptide Profiles in Chronic Hypertension by Single or Sequentially Combined Renovascular and DOCA-Salt Treatments

2021 ◽  
Vol 12 ◽  
Author(s):  
Carolina S. Cerrudo ◽  
Susana Cavallero ◽  
Martín Rodríguez Fermepín ◽  
Germán E. González ◽  
Martín Donato ◽  
...  
Keyword(s):  
Gene Expression ◽  
Left Ventricular Hypertrophy ◽  
Cardiac Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Prolonged Treatment ◽  
Chronic Hypertension ◽  
Peptide Profiles

The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) during 6 and 12 weeks of treatment. We also studied the consecutive combination of both models in inverse sequences: RV 6 weeks/DS 6 weeks and DS 6 weeks/RV 6 weeks. All treated groups developed hypertension. Cardiac hypertrophy and left ventricular ANP gene expression were more pronounced in single DS than in single RV groups. BNP gene expression was positively correlated with left ventricular hypertrophy only in RV groups, while ANP gene expression was positively correlated with left ventricular hypertrophy only in DS groups. Combined models exhibited intermediate values between those of single groups at 6 and 12 weeks. The latter stimulus associated to the second applied overload is less effective than the former to trigger cardiac hypertrophy and to increase ANP and BNP gene expression. In addition, we suggest a correlation of ANP synthesis with volume overload and of BNP synthesis with pressure overload-induced hypertrophy after a prolonged treatment. Volume and pressure overload may be two mechanisms, among others, involved in the differential regulation of ANP and BNP gene expression in hypertrophied left ventricles. Plasma ANP levels reflect a response to plasma volume increase and volume overload, while circulating BNP levels seem to be regulated by cardiac BNP synthesis and ventricular hypertrophy.

Ventricular adrenomedullin concentration is a sensitive biochemical marker for volume and pressure overload in rats

2000 ◽  
Vol 278 (2) ◽  
pp. H633-H642 ◽  
Author(s):  
Fumiki Yoshihara ◽  
Toshio Nishikimi ◽  
Takeshi Horio ◽  
Chikao Yutani ◽  
Noritoshi Nagaya ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Cardiac Hypertrophy ◽  
Heavy Chain ◽  
Biochemical Marker ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Mrna Isoforms ◽  
The Creation ◽  
The Right

This study was designed to investigate the pathophysiological significance of adrenomedullin (AM) concentration in volume- and pressure-overloaded cardiac hypertrophy. We measured ventricular AM concentrations and compared them with changes of α-actin and myosin heavy chain (MHC) mRNA isoforms after the creation of an aortocaval (AC) shunt as a volume-overload model or the injection of monocrotaline (MCT) as a pressure-overload model, respectively. The left ventricular AM levels after the creation of AC shunt and the right ventricular AM levels after the injection of MCT were significantly increased and correlated with changes of the α-actin and MHC mRNA isoforms. However, the ventricular AM mRNA expressions were increased and correlated with ventricular AM concentrations only in the AC shunt model. These results suggest that the ventricular AM levels are upregulated in both the volume- and pressure-overloaded cardiac hypertrophy by differential transcriptional regulation and that the ventricular AM may be a biochemical marker for the volume and pressure overload to the ventricle.

Endothelin-1 and its binding sites are upregulated in pressure overload cardiac hypertrophy

1995 ◽  
Vol 268 (5) ◽  
pp. H2084-H2091 ◽  
Author(s):  
M. Arai ◽  
A. Yoguchi ◽  
T. Iso ◽  
T. Takahashi ◽  
S. Imai ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Binding Sites ◽  
Pressure Overload ◽  
Sham Operation ◽  
Endothelin 1 ◽  
Important Relationship ◽  
Mrna Hybridization ◽  
In Situ Mrna Hybridization

The purpose of this study was to determine whether endothelin and endothelin receptors play an important role in the development of cardiac hypertrophy due to pressure overload in vivo. Cardiac hypertrophy was produced by placing a constricting clip around the suprarenal abdominal aorta of rats. Hemodynamic parameters and plasma and ventricular concentrations of endothelin-1 (ET-1) were measured in control unoperated rats, and 30 min, 2 and 6 h, and 1 and 8 days after operation in pressure overload rats and sham-operated rats. The density and dissociation constant of ET-1 binding sites were also measured in control rats and 1 and 8 days after pressure overload and sham operation. Additionally, in situ mRNA hybridization for preproendothelin-1 (preproET-1) mRNA was performed to determine which cells were responsible for increased ET-1 levels. Ventricular ET-1 levels increased markedly on day 8 of pressure overload, whereas plasma ET-1 levels increased transiently only 30 min after operation, quickly returning to control level. In addition, ventricular ET-1 levels on day 8 showed a significant positive correlation with the degree of cardiac hypertrophy. In situ mRNA hybridization revealed that cardiac myocytes expressed preproET-1 mRNA in hypertrophied hearts in vivo. In accord with the elevation of ventricular ET-1 levels, the density of ET-1 binding sites was increased significantly, without affecting their binding affinity, on day 8 of pressure overload. These data are compatible with the hypothesis that increases in locally produced ET-1 and the density of ET-1 binding sites have an important relationship with the development of cardiac hypertrophy in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

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