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.

Left ventricular hypertrophy due to volume overload versus pressure overload

1992 ◽  
Vol 263 (4) ◽  
pp. H1137-H1144 ◽  
Author(s):  
B. A. Carabello ◽  
M. R. Zile ◽  
R. Tanaka ◽  
G. Cooper
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Contractile Function ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Compensatory Hypertrophy ◽  
Similar Amount ◽  
Stroke Work ◽  
Hypertrophic Response

Left ventricular hemodynamic overload produces an increase in stroke work (SW), which is compensated by the development of left ventricular hypertrophy. However, recent reports question the adequacy of this compensation in mitral regurgitation (MR). Accordingly, we examined the adequacy of compensatory hypertrophy in chronic experimental MR. Six dogs with chronic severe MR were matched according to SW with six dogs that had severe chronic aortic stenosis (ASSW). SW in the two groups was increased identically (40%) compared with normals. However, the hypertrophic response was much greater in the AS group [left ventricular wt (g) to body wt (kg) ratio (LVBW) 4.0 +/- 0.2 normals, 5.0 +/- 0.2 MR, and 7.5 +/- 0.2 ASSW; P < 0.05 MR vs. ASSW]. This differing hypertrophic response increased normalized SW, the area within the stress-volume loop, in MR (90 +/- 5 g) vs. 63 +/- 5 g in ASSW (P < 0.05). Thus in MR, each unit of myocardium had to perform more work than in AS. In a separate comparison, four different dogs with AS (ASHy), which had a similar amount of hypertrophy to the MR dogs (LVBW) (5.0 +/- 0.2 MR, 5.2 +/- 0.2 ASHy) were studied. SW was greater in the MR group, suggesting more SW overload was required to produce similar amounts of hypertrophy in MR vs. AS. Contractile function was depressed in the MR group but not in the AS. These findings indicate that the hypertrophic response to a similar SW demand is less in MR than AS, a response associated with contractile dysfunction in the MR group.

Myocardial and Coronary Effects of Propofol in Rabbits with Compensated Cardiac Hypertrophy

2001 ◽  
Vol 95 (3) ◽  
pp. 699-707 ◽  
Author(s):  
Alexandre Ouattara ◽  
Olivier Langeron ◽  
Rachid Souktani ◽  
Stéphane Mouren ◽  
Pierre Coriat ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Cardiac Hypertrophy ◽  
Myocardial Contractility ◽  
Ventricular Hypertrophy ◽  
Sham Group ◽  
Systolic Function ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Perfused Heart ◽  
Diastolic Compliance

Background Myocardial effects of propofol have been previously investigated but most studies have been performed in healthy hearts. This study compared the cardiac effects of propofol on isolated normal and hypertrophic rabbits hearts. Methods The effects of propofol (10-1,000 microM) on myocardial contractility, relaxation, coronary flow and oxygen consumption were investigated in hearts from rabbits with pressure overload-induced left ventricular hypertrophy (LVH group, n = 20) after aortic abdominal banding and from sham-operated control rabbits (SHAM group, n = 10), using an isolated and erythrocyte-perfused heart model. In addition, to assess the myocardial and coronary effects of propofol in more severe LVH, hearts with a degree of hypertrophy greater than 140% were selected (severe LVH group, n = 7). Results The cardiac hypertrophy model induced significant left ventricular hypertrophy (136+/-21%, P &lt; 0.05). The pressure-volume relation showed normal systolic function but an altered diastolic compliance in hypertrophic hearts. Propofol only decreased myocardial contractility and relaxation at supratherapeutic concentrations (&gt; or = 300 microM) in SHAM and LVH groups. The decrease in myocardial performances was not significantly different in SHAM and LVH groups. Propofol induced a significant increase in coronary blood flow which was not significantly different between groups. In severe LVH group, the degree of hypertrophy reached to 157+/-23%. Similarly, the effects of concentrations of propofol were not significantly different from the SHAM group. Conclusions Propofol only decreased myocardial function at supratherapeutic concentrations. The myocardial and coronary effects of propofol were not significantly modified in cardiac hypertrophy.

scholarly journals Cardiomyocyte loss is not required for the progression of left ventricular hypertrophy induced by pressure overload in female mice

2016 ◽  
Vol 229 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Julia Schipke ◽  
Clara Grimm ◽  
Georg Arnstein ◽  
Jens Kockskämper ◽  
Simon Sedej ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Female Mice

Correlation between Hypervolemia, Left Ventricular Hypertrophy and Fibroblast Growth Factor- 23 in Prevalent Hemodialysis Patients

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Sahar Mahmoud Shawky ◽  
Mohamed Saeed Hassan ◽  
Maha Mohamed Khalifa ◽  
Kholoud Mahmoud Amin
Keyword(s):  
Weight Gain ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Volume Overload ◽  
Hemodialysis Patients ◽  
Left Ventricular ◽  
Bone Diseases ◽  
Interdialytic Weight Gain ◽  
Fgf 23 ◽  
Esrd Patients

Abstract Background Patients with end-stage renal disease are exposed to extreme volume shifts and thereby cardiovascular strain as a consequence of interdialytic weight gain, fluid removal during hemodialysis and also chronic fluid overload. In long-term hemodialysis patients, higher IDWG (interdialytic weight gain) is associated with poor survival and increased cardiovascular death. Patients with the lowest interdialytic fluid retention have the greatest survival. It was found that increased interdialytic volume load is associated with increased both LVMI and FGF-23 level. Objective To evaluate correlation between hypervolemia, left ventricular hypertrophy and FGF-23 in prevalent hemodialysis patients. Patients and Methods This cross sectional study was conducted in Ain shams university hospital and Al Agoza hospital, on 60 prevalent hemodialysis patients.Three patient died during the study. Results FGF-23 had a positive correlation with (weight gain, (PO4)3-, PTH, IVS, PW and LVMI). Conclusion FGF-23 might be a marker of volume overload and LVH in ESRD patients, as it positively correlated with (weight gain, IVS, PW and LVMI). FGF-23 is a marker of bone diseases, as it positively correlated with (PO4)3- and PTH. Volume overload has a negative impact on morbidity and mortality in ESRD patients.

Role of Calcineurin-Dependent Signaling Pathway on the Left Ventricular Hypertrophy Induced by Pressure Overload

2001 ◽  
Vol 31 (11) ◽  
pp. 1159
Author(s):  
Hainan Piao ◽  
Jin Sook Kwon ◽  
Hye Young Lee ◽  
Tae Jin Youn ◽  
Dong Woon Kim ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Signaling Pathway ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Dependent Signaling Pathway

39 Pressure-overload left ventricular hypertrophy in the rat

1993 ◽  
Vol 11 (11) ◽  
pp. 1314
Author(s):  
J. F. Viallard ◽  
P. Dos-Santos ◽  
G. Raffard ◽  
L. Tariosse ◽  
G. Gouverneur ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular
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