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.

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.

scholarly journals D-Shaped Left Ventricle, Anatomic, and Physiologic Implications

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Eder Hans Cativo Calderon ◽  
Tuoyo O. Mene-Afejuku ◽  
Rachna Valvani ◽  
Diana P. Cativo ◽  
Devendra Tripathi ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Interventricular Septum ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Transthoracic Echocardiogram ◽  
Elderly Male ◽  
In Series ◽  
The Right

Right ventricular loading/pressure influences left ventricular function because the two ventricles pump in series and because they are anatomically arranged in parallel, sharing the common ventricular septum. Flattening of the interventricular septum detected during echocardiographic examination is called D-shaped left ventricle. We present a case of an elderly male of African descent, who presented with increased shortness of breath. Transthoracic echocardiogram showed flattening and left sided deviation of interventricular septum causing a decreased size in left ventricle, secondary to volume/pressure overload in the right ventricle. While patient received hemodialysis therapy and intravascular volume was removed, patient blood pressure was noted to increase, paradox. Repeated transthoracic echocardiogram demonstrated less left deviation of interventricular septum compared with previous echocardiogram. We consider that it is important for all physicians to be aware of the anatomic and physiologic implication of D-shaped left ventricle and how right ventricle pressure/volume overload affects its function and anatomy.

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)

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

1994 ◽  
Vol 266 (1) ◽  
pp. H68-H78 ◽  
Author(s):  
C. R. Cory ◽  
R. W. Grange ◽  
M. E. Houston
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Pressure Overload ◽  
Fold Increase ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Tension Development ◽  
Sequestration Potential

The loss of load-sensitive relaxation observed in the pressure-overloaded heart may reflect a strategy of slowed cytosolic Ca2+ uptake to yield a prolongation of the active state of the muscle and a decrease in cellular energy expenditure. A decrease in the potential of the sarcoplasmic reticulum (SR) to resequester cytosolic Ca2+ during diastole could contribute to this attenuated load sensitivity. To test this hypothesis, both in vitro mechanical function of anterior papillary muscles and the SR Ca2+ sequestration potential of female guinea pig left ventricle were compared in cardiac hypertrophy (Hyp) and sham-operated (Sham) groups. Twenty-one days of pressure overload induced by coarctation of the suprarenal, subdiaphragmatic aorta resulted in a 36% increase in left ventricular mass in the Hyp. Peak isometric tension, the rate of isometric tension development, and the maximal rates of isometric and isotonic relaxation were significantly reduced in Hyp. Load-sensitive relaxation were significantly reduced in Hyp. Load-sensitive relaxation quantified by the ratio of a rapid loading to unloading force step in isotonically contracting papillary muscle was reduced 50% in Hyp muscles. Maximum activity of SR Ca(2+)-adenosinetriphosphatase (ATPase) measured under optimal conditions (37 degrees C; saturating Ca2+) was unaltered, but at low free Ca2+ concentrations (0.65 microM), it was decreased by 43% of the Sham response. Bivariate regression analysis revealed a significant (r = 0.84; P = 0.009) relationship between the decrease in SR Ca(2+)-ATPase activity and the loss of load-sensitive relaxation after aortic coarctation. Stimulation of the SR Ca(2+)-ATPase by the catalytic subunit of adenosine 3',5'-cyclic monophosphate-dependent protein kinase resulted in a 2.6-fold increase for Sham but only a 1.6-fold increase for Hyp. Semiquantitative Western blot radioimmunoassays revealed that the changes in SR Ca(2+)-ATPase activity were not due to decreases in the content of the Ca(2+)-ATPase protein or phospholamban. Our data directly implicate a role for decreased SR function in attenuated load sensitivity. A purposeful downregulation of SR Ca2+ uptake likely results from a qualitative rather than a quantitative change in the ATPase and possibly one of its key regulators, phospholamban.

scholarly journals Leonurine Attenuates Pressure-Overload Cardiac Hypertrophy Induced By Abdominal Aortic Constriction In Rats

2021 ◽  
Author(s):  
Ding Xiaoli ◽  
Yuan Qingqing ◽  
Qian Haibing
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Ang Ii ◽  
Aortic Constriction ◽  
Qrt Pcr ◽  
Abdominal Aortic

Abstract Background: Myocardial hypertrophy occurs in many cardiovascular diseases. Leonurine (Leo) is commonly used for cardiovascular and cerebrovascular diseases. However, whether it can prevent cardiac hypertrophy is not known. The aim of this study was to investigate the effect and mechanism of Leonurine (Leo) against pressure-overload cardiac hypertrophy induced by abdominal aortic constriction (AAC) in rats. Methods: To answer this question, we prove it in the following way: Cardiac function was evaluated by hemodynamic; the left ventricle enlargement was measured by heart weight index (HWI) and left ventricular mass index (LVWI); myocardial tissue changes and myocardial cell diameter (MD) were determined by Hematoxylin and eosin (HE) staining; theβ-myosin heavy chain(β-MHC)and atrial natriuretic factor (ANF), which are recognized as a marker of cardiac hypertrophy, were determined by Real-time quantitative PCR (qRT-PCR), then another gene phospholipase C (PLC), inositol triphosphate (IP3), which associated with RAS were determined by Western blot(WB). angiotensin II (Ang II), angiotensin II type 1 receptor (AT1R) were determined by ELISA, WB and qRT-PCR methods. Finally, we measured the level of Ca2+ by microplate method and the protooncogene c-fos and c-myc mRNA in left ventricular myocardium by qRT-PCR.Results: Compare with control group, Leonurine can improve systolic dysfunction; inhibit the increase of left cardiac; inhibit myocardial cells were abnormally large and restrain the changes of cardiac histopathology; decrease the expression of β-MHC, ANF, Ang II, AT1R, c-fos and c-myc mRNA and the protein levels of PLC, IP3, AngII and AT1R in left ventricular myocardium, in addition, the content of Ca2+ also decrease. Conclusion: Therefore, Leonurine can inhibit cardiac hypertrophy induced by AAC and its effects may be associated with RAS.

Abstract 18822: Endoglin Selectively Modulates TRPC Expression in Response to Left or Right Ventricular Pressure Overload

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Kevin J Morine ◽  
Vikram Paruchuri ◽  
Xiaoying Qiao ◽  
Duc T Pham ◽  
Gordon S Huggins ◽  
...  
Keyword(s):  
Transforming Growth Factor Beta ◽  
Cardiac Fibrosis ◽  
Transient Receptor Potential ◽  
Transforming Growth Factor ◽  
Pressure Overload ◽  
Receptor Potential ◽  
Left Ventricular ◽  
Transient Receptor ◽  
Novel Target ◽  
The Right

Introduction: Endoglin is an accessory receptor for the cytokine transforming growth factor beta. Reduced endoglin activity limits cardiac fibrosis due to left ventricular (LV) pressure overload. Recently, we reported that reducing endoglin activity also limits upregulation of the profibrogenic transient receptor potential canonical channel 6 (TRPC6) in the right ventricle (RV) during pressure overload. Few studies have compared TRPC channel expression in the RV versus LV. Hypothesis: We hypothesized that endoglin regulates TRPC upregulation in response to RV and LV pressure overload. Methods: To explore a functional role for endoglin as a regulator of TRPC expression in response to RV or LV pressure overload, endoglin haploinsufficient (Eng+/-) and wild-type (Eng+/+) mice were exposed to thoracic aortic (TAC) or pulmonary arterial (PAC) constriction for 10 weeks. Biventricular tissue was then analyzed by real-time polymerase chain reaction. Results: After TAC, LV levels of TPRC1 and 6 were increased in both Eng +/+ and Eng +/- mice compared to sham controls. LV levels of TRPC4 were increased in Eng +/+, not Eng +/- mice after TAC. After PAC, RV levels of TRPC1, 3, 4, and 6 were increased in Eng +/+ compared to sham controls. In contrast, chronic RV pressure overload did not increase RV levels of TRPC1, 3, 4, and 6 in Eng +/- mice compared to sham controls. Conclusions: Pressure overload induces distinct profiles of TRPC expression in the RV and LV and these effects in the RV require full endoglin activity. Taken together, these data support that endoglin may be an important and novel target of therapy to modulate RV responses to injury.

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