Moderate Resistance Training Attenuates the Increase in Blood Pressure and Decreases the Cardiomyocyte Nuclei Number in Hypertensive Rats (original) (raw)
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Temporal characteristics of cardiomyocyte hypertrophy in spontaneously hypertensive rats
Cardiovascular Pathology
Background: The spontaneously hypertensive rat (SHR) is frequently used as model of cardiovascular disease, with considerable disparity in reported parameters of hypertrophy. The aim of this study was to assess the temporal changes occurring during the development and progression of cardiomyocyte hypertrophy in SHR, subsequent to pressure overload, compared to changes associated with normal aging using the normotensive Wistar-Kyoto (WKY) rat. Methods: Ventricular cardiomyocytes were isolated from rats at 8, 12, 16, 20 and 24 weeks, and parameters of hypertrophy (cell dimensions, protein mass, de novo protein synthesis, and gene expression) and function (contraction and hypertrophic responsiveness in vitro) were assessed. Results: Hypertension was evident at z7 weeks in SHRs. Heart:body mass ratio, cardiomyocyte protein mass and width were elevated (P < .05) in SHRs at 16-20 weeks compared to WKYs. In SHRs compared to WKYs at 16 weeks, there was a transient increase (P < .05) in protein synthesis, enhanced hypertrophic responsiveness to phorbol-12-myristate-13-acetate, and induced hypertrophic responsiveness to isoprenaline. Skeletal-a-actin mRNA was detected in SHR but not WKY cells at all ages. ANP mRNA was lower in SHR than in WKY cells at 8-20, but progressively increased (P < .05) from 12 to 24 weeks within SHRs. Contractile function increased (P < .05) at 20 weeks in SHR compared to WKY rats. Conclusion: Structural and functional changes occurring at the cellular level in the myocardium of SHR follow a distinct pattern, such that pressure overload was initially accompanied by expressional changes (8-12 weeks), followed by active hypertrophic growth and enhanced function (16-20 weeks), which subsequently decelerated as stable compensation was attained.
Journal of Applied Physiology, 2007
Exercise training and hypertension induced cardiac hypertrophy but modulate differently left ventricle (LV) function. This study set out to evaluate cardiac adaptations induced by moderate exercise training in normotensive and untreated severe hypertensive rats. Four groups of animals were studied: normotensive (Ctl) and severe hypertensive (HT) Wistar rats were assigned to be sedentary (Sed) or perform a moderate exercise training (Ex) over a 10-wk period. Severe hypertension was induced in rat by a two-kidney, one-clip model. At the end of the training period, hemodynamic parameters and LV morphology and function were assessed using catheterism and conventional pulsed Doppler echocardiography. LV histology was performed to study fibrosis infiltrations. Severe hypertension increased systolic blood pressure to 202 ± 9 mmHg and induced pathological hypertrophy (LV hypertrophy index was 0.34 ± 0.02 vs. 0.44 ± 0.02 in Ctl-Sed and HT-Sed groups, respectively) with LV relaxation alterati...
Hypertension, 2009
The effect of endurance training (swimming 90 min/d for 5 days a week for 60 days) on cardiac hypertrophy was investigated in the spontaneously hypertensive rat (SHR). Sedentary SHRs (SHR-Cs) and normotensive Wistar rats were used as controls. Exercise training enhanced myocardial hypertrophy assessed by left ventricular weight/tibial length (228Ϯ7 versus 251Ϯ5 mg/cm in SHR-Cs and exercised SHRs [SHR-Es], respectively). Myocyte cross-sectional area increased Ϸ40%, collagen volume fraction decreased Ϸ50%, and capillary density increased Ϸ45% in SHR-Es compared with SHR-Cs. The mRNA abundance of atrial natriuretic factor and myosin light chain 2 was decreased by the swimming routine (100Ϯ19% versus 41Ϯ10% and 100Ϯ8% versus 61Ϯ9% for atrial natriuretic factor and myosin light chain 2 in SHR-Cs and SHR-Es, respectively). The expression of sarcoplasmic reticulum Ca 2ϩ pump was significantly augmented, whereas that of Na ϩ /Ca 2ϩ exchanger was unchanged (93Ϯ7% versus 167Ϯ8% and 158Ϯ13% versus 157Ϯ7%, sarcoplasmic reticulum Ca 2ϩ pump and Na ϩ /Ca 2ϩ exchanger in SHR-Cs and SHR-Es, respectively; PϽ0.05). Endurance training inhibited apoptosis, as reflected by a decrease in caspase 3 activation and poly(ADP-ribose) polymerase-1 cleavage, and normalized calcineurin activity without inducing significant changes in the phosphatidylinositol 3-kinase/Akt pathway. The swimming routine improved midventricular shortening determined by echocardiography (32.4Ϯ0.9% versus 36.9Ϯ1.1% in SHR-Cs and SHR-Es, respectively; PϽ0.05) and decreased the left ventricular free wall thickness/left ventricular cavity radius toward an eccentric model of cardiac hypertrophy (0.59Ϯ0.02 versus 0.53Ϯ0.01 in SHR-Cs and SHR-Es, respectively; PϽ0.05). In conclusion, we present data demonstrating the effectiveness of endurance training to convert pathological into physiological hypertrophy improving cardiac performance. The reduction of myocardial fibrosis and calcineurin activity plus the increase in capillary density represent factors to be considered in determining this beneficial effect. (Hypertension. 2009;53:708-714.)
Left ventricular remodeling with exercise in hypertension
AJP: Heart and Circulatory Physiology, 2009
We investigated how exercise training superimposed on chronic hypertension impacted left ventricular remodeling. Cardiomyocyte hypertrophy, apoptosis, and proliferation in hearts from female spontaneously hypertensive rats (SHRs) were examined. Four-month-old SHR animals were placed into a sedentary group (SHR-SED; n = 18) or a treadmill running group (SHR-TRD, 20 m/min, 1 h/day, 5 days/wk, 12 wk; n = 18). Age-matched, sedentary Wistar Kyoto (WKY) rats were controls ( n = 18). Heart weight was greater in SHR-TRD vs. both WKY ( P < 0.01) and SHR-SED ( P < 0.05). Morphometric-derived left ventricular anterior, posterior, and septal wall thickness were increased in SHR-SED relative to WKY and augmented in SHR-TRD. Cardiomyocyte surface area, length, and width were increased in SHR-SED relative to WKY and further increased in SHR-TRD. Calcineurin abundance was increased in SHR-SED vs. WKY ( P < 0.001) and attenuated in SHR-TRD relative to SHR-SED ( P < 0.05). Protein abundan...
Myocardial hypertrophy of normotensive Wistar-Kyoto rats
AJP: Heart and Circulatory Physiology, 2003
In our studies with spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), and Wistar rats, we observed normotensive WKY rats with cardiac hypertrophy determined by a greater left ventricular (LV) mass (LVM)-to-body weight (BW) ratio (LVM/BW) than that of normotensive Wistar rats. Thus we compared the following parameters in SHR, WKY, and Wistar rats: LVM/BW, cell capacitance as index of total surface area of the myocytes, length, width, and cross-sectional area of cardiac myocytes, LV collagen volume fraction, and myocardial stiffness. The LVM/BW of WKY (2.41 ± 0.03 mg/g, n = 41) was intermediate between SHR (2.82 ± 0.04 mg/g, n = 47) and Wistar rats (1.98 ± 0.04 mg/g, n = 28). A positive correlation between blood pressure and LVM was found in SHR, whereas no such relationship was observed in WKY or Wistar rats. Cell capacitance and cross-sectional area were not significantly different in SHR and WKY rats; these values were significantly higher than those of Wistar rats. The cell le...
2010
Sprint training attenuates myocyte hypertrophy and improves Ca 2ϩ homeostasis in postinfarction myocytes. J. Appl. Physiol. 84(2): 544-552, 1998.-Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na ϩ /Ca 2ϩ exchange currents (I Na/Ca ; 3 Na ϩ out:1 Ca 2ϩ in) and sarcoplasmic reticulum (SR)-releasable Ca 2ϩ contents. These defects in Ca 2ϩ regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca 2ϩ regulation, the present study examined whether 6-8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac ␣-myosin heavy chain (MHC) isoforms (57.2 Ϯ 1.9 vs. 49.3 Ϯ 3.5 in MI-HIST vs. MI-Sed, respectively; P Յ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 Ϯ 4 vs. 130 Ϯ 5 µm in MI-HIST vs. MI-Sed, respectively; P Յ 0.005) and cell capacitances (212 Ϯ 8 vs. 242 Ϯ 9 pF in MI-HIST vs. MI-Sed, respectively; P Յ 0.015). Reverse I Na/Ca was significantly lower (P Յ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse I Na/Ca (P Յ 0.05) without affecting the amount of Na ϩ /Ca 2ϩ exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca 2ϩ content, as estimated by integrating forward I Na/Ca during caffeine-induced SR Ca 2ϩ release, was also significantly increased (P Յ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.
Nutrition Research, 2006
Several studies have shown alterations in hearts from animals subjected to food restriction (FR). However, few experiments in hearts evaluating pressure overload have been reported. We examined the effects of chronic FR on myocardial function and morphology in spontaneously hypertensive rats (SHR). Sixty-day-old SHR were fed a control (C) or a restricted diet (daily intake reduced to 50% of amount of food consumed by the control group) for 90 days. Myocardial performance was studied in isolated left ventricular (LV) papillary muscle. Food restriction decreased body weight and LV weight; LV weight/body-weight ratio was lower in the food-restricted group (SHR-C, 2.84 F 0.21 mg/g; SHR-FR, 2.56 F 0.24 mg/g; P b .05). Food restriction did not change arterial systolic blood pressure. Myocyte surface area was lower in the food-restricted group ( P b .01). Food restriction induced myocardial ultrastructural alterations including reduced sarcoplasm content, reduced and disorganized myofilaments, disorganized Z line, dilated sarcoplasmic reticulum, and deep infoldings of plasma membrane. Myocardial hydroxyproline concentration was increased in the restricted rats. Peak developed tension ( P b .05) and maximum rate of tension development ( P b .01) were decreased in the SHR-FR group. In conclusion, myocardium of SHR subjected to chronic FR presents attenuation of hypertrophy development, ultrastructural changes, increased collagen content, and systolic dysfunction. D
Experimental Physiology, 2008
In the present study we investigated the effects of physical training on plasma and cardiac angiotensin(1-7) [Ang(1-7)] levels. In addition, possible changes in expression of the Ang(1-7) Mas receptor in the heart were also evaluated. Normotensive Wistar rats and spontaneously hypertensive rats (SHR) were subjected to an 8 week period of 5% overload swimming training. Blood pressure was determined by a tail-cuff system. Heart and left ventricle weights and cardiomyocyte diameter were analysed to evaluate cardiac hypertrophy. Radioimmunoassay was used to measure angiotensin levels. levels. No significant changes were observed in plasma Ang(1-7) and left ventricular Ang II concentrations in either strain. Furthermore, Mas mRNA and protein expression in left ventricle were substantially increased in trained SHR. The physical training protocol used did not change blood pressure in either strain. These results suggest that the beneficial effects induced by swimming training in hypertensive rats might include an augmentation of Ang(1-7) and its receptor in the heart.
Hypertension, 2001
Whether left ventricular (LV) hypertrophy is important in the development of LV failure associated with advanced myocardial damage and detrimental chamber and interstitial remodeling in hypertension has not been established. We examined the effect of an antihypertensive agent without the ability to regress LV hypertrophy on the development of LV changes in spontaneously hypertensive rats (SHR). Hydralazine given to SHR from 5.2 to 26 months of age returned systolic blood pressure to Wistar Kyoto (WKY) control values but failed to prevent the increase in LV mass noted in SHR (at 26 months of age: WKY, 0.99±0.02 g; untreated SHR, 1.40±0.02 g; treated SHR, 1.36±0.02 g; P <0.001 in SHR versus WKY). In comparison to both 16-month-old SHR and age-matched WKY, 26-month-old untreated SHR developed signs consistent with heart failure, LV dilatation (an increased LV internal radius), an eccentric LV geometry, advanced myocyte necrosis, an increase in myocardial collagen solubility (an inde...