scholarly journals Osteopontin Modulates Myocardial Hypertrophy in Response to Chronic Pressure Overload in Mice

Hypertension ◽  
2004 ◽  
Vol 44 (6) ◽  
pp. 826-831 ◽  
Author(s):  
Zhonglin Xie ◽  
Mahipal Singh ◽  
Krishna Singh
1982 ◽  
Vol 242 (5) ◽  
pp. H882-H889 ◽  
Author(s):  
J. M. Capasso ◽  
J. E. Strobeck ◽  
A. Malhotra ◽  
J. Scheuer ◽  
E. H. Sonnenblick

The effects of renovascular hypertension and its reversal on the contractile performance of papillary muscles from rats has been examined. Hypertension of 10 wk duration caused a 48% increase in heart weight and significant prolongations of isometric time to peak tension (TPT), time to half relaxation, and time to peak shortening (TPS). A significant depression in the velocity of shortening was observed in the 10-wk group. However, muscles from hypertensive rats were still able to maintain normal levels of peak isometric developed tension and peak shortening; this may be due to the observed prolongation of TPT and TPS, respectively. In addition, calcium-activated actomyosin ATPase activity was depressed in hearts of hypertensive animals. Reversal of hypertension was studied at 20 wk after the onset of hypertension (10 wk of hypertension followed by 10 wk of normotension). Contractile and biochemical alterations observed in hypertensive animals were reversed in rats undergoing this regime. Thus reversal of a gradually applied pressure overload resulted in the regression of mechanical and biochemical abnormalities associated with the pressure overload myocardial hypertrophy.


2018 ◽  
Vol 3 (66) ◽  
Author(s):  
Tomas Venckūnas ◽  
Birutė Mažutaitienė ◽  
Arvydas Stasiulis

Endurance running is an exercise practiced by athletes in many sports. Being benefi cial to health, it is also under-taken by a great number of non-athletic individuals. Rigorous endurance training frequently induces symmetric (i. e. both ventricular chamber dilation and wall thickening) myocardial hypertrophy, which is a physiological adapta-tion. Although distance running is a sport associated with haemodynamic volume rather than pressure overload, in addition to enlarged cardiac output, systolic arterial blood pressure also considerably increases during running. The extent of the cardiac hypertrophy was shown to be correlated with peak blood pressure measured during laboratory exercise. However, the predominant type of myocardial hypertrophy (the ratio between the myocardial wall thickness and chamber size) in endurance runners remains contradictory, and the majority of the responsible factors are still to be determined. The aim of this study was to determine possible correlations between post-run systolic blood pressure and myocardial hypertrophy in endurance runners.Standard transthoracic two-dimensional M-mode echocardiography was performed in white adult male distance runners (n = 49) of national level within four weeks of treadmill testing, which was a non-continuous incremental exercise test employed for the determination of the heart rate as well as post-exertional systolic blood pressure re-sponse. Runners’ training volume (evaluated as the average number of hours per week spent training averaged over the past four weeks) correlated (p < 0.05) positively with the left ventricular (LV) wall thickness but not with the cavity size or LV mass (p > 0.05). Training volume also positively correlated with systolic blood pressure response to exercise (p < 0.05), but negatively with submaximal exercise heart rate (p < 0.01). Post-run systolic blood pressure correlated positively with LV wall thickness and LV concentricity (namely, the ratio between the myocardial wall thick-ness and chamber size) (p < 0.05), but no signifi cant correlation of any of the LV size parameters with resting heart rate, blood pressure, or systolic blood pressure in 2 to 4 min during the recovery period was revealed. Submaximal and maximal heart rate correlated signifi cantly and negatively with LV wall thickness, LV mass, and systolic blood pressure measured immediately after running (p < 0.05).Training volume and post-run systolic blood pressure have been found to correlate positively with LV wall thickness and concentricity in white adult male distance runners. Negative correlation of exercise heart rate has been found with the post-exercise systolic blood pressure, LV wall thickness, and LV mass.Keywords: myocardial hypertrophy, pressure overload, echocardiography, athlete’s heart.


2018 ◽  
Vol 120 ◽  
pp. 13
Author(s):  
M. Ruppert ◽  
S. Korkmaz-Icöz ◽  
S. Loganathan ◽  
W. Jiang ◽  
L. Lehmann ◽  
...  

2013 ◽  
Vol 168 (3) ◽  
pp. 2049-2056 ◽  
Author(s):  
Jørgen Gravning ◽  
Mohammed Shakil Ahmed ◽  
Thomas G. von Lueder ◽  
Thor Edvardsen ◽  
Håvard Attramadal

2019 ◽  
Vol 22 (6) ◽  
pp. E432-E437
Author(s):  
Zhixiang Xie ◽  
Shuyin Wang ◽  
Zijing Liang ◽  
Liangbo Zeng ◽  
Rongde Lai ◽  
...  

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.


1994 ◽  
Vol 266 (5) ◽  
pp. H1738-H1745 ◽  
Author(s):  
Q. Li ◽  
E. C. Keung

In the one-clip, two-kidney model of hypertensive rat, a gradual chronic pressure overload is imposed on the heart. Myocardial hypertrophy resulting from such pressure overload is associated with an increased but slower inactivating L-type calcium current and prolongation of action potential duration. Voltage clamp experiments in a variety of excitable tissues indicate that a 4-aminopyridine-sensitive transient outward current (Ito) plays an important role in regulating the action potential duration. Accordingly, we studied Ito in single adult cardiac myocytes enzymatically isolated from hypertrophied left ventricles of the renovascular hypertensive (HBP) rat hearts using the whole cell patch-clamp method. The current densities (normalized to cell capacitative surface area) measured at the early transient peak Ito, at the steady state, and as the difference between the transient peak and the steady state were larger in HBP cells (n = 23) than in control (Ctrl) cells (n = 20) (P < 0.05). There was no difference in the Ito reversal potential between Ctrl (-60.9 +/- 1.9 mV, mean +/- SE; n = 16) and HBP (-63.7 +/- 2.6 mV; n = 19) cells. The observed increase in Ito amplitude was not due to an increase in the number of channels available for activation or in the fraction of channels activated because there were no statistical differences in the membrane potential at which one-half of the Ito channels are activated (V0.5) for the steady-state activation and inactivation curves between Ctrl and HBP cells. The time course of inactivation of Ito was described by a double-exponential function.(ABSTRACT TRUNCATED AT 250 WORDS)


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