Faculty Opinions recommendation of Adverse cardiac remodelling in spontaneously hypertensive rats: acceleration by high aerobic exercise intensity.

AbstractBackground and Purpose. In order to explore the possible effects of physical therapy interventions on patients with hypertension, we evaluated the effects of aerobic exercise training on myocardial energy metabolism in an animal model of hypertension. Subjects. We used 36 female spontaneously hypertensive rats (rats with genetically induced hypertension) and 12 normotensive Wistar-Kyoto rats. Methods. The normotensive rats were sedentary and formed the CONsed group. The spontaneously hypertensive rats were randomly divided into 3 experimental groups (12 rats per group). Hypertensive rats that were sedentary formed the HTNsed group, those that received 8 weeks of exercise training formed the HTN×8 group, and those that received 16 weeks of exercise training formed the HTN×16 group. We measured systolic blood pressure, heart wet weight, maximal activities of cardiac energy metabolism enzymes, glucose transporter content, and total concentrations of protein, glycogen, and triglyceride. Results. Systolic blood pressure was greater than 200 mm Hg in the CONsed group at the time of testing. Exercise training modestly (∼11–18 mm Hg) lowered blood pressure in the HTN×8 and HTN×16 groups. Fatty acid enzyme activity was greater in the CONsed group than in the HTNsed and HTN×8 groups, but activity was roughly equivalent between the CONsed group and the HTN×16 group. Glucose enzyme activity was greater in the HTN×16 group than in the CONsed group and the HTNsed group. Intracellular glycogen concentration was greater in the HTN×8 group than in the HTNsed group. Discussion and Conclusion. Results of this study suggest that aerobic exercise training may help to normalize cardiac energy metabolism in mammals with hypertension.

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Contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats

Clinical Science ◽

10.1042/cs0970239 ◽

1999 ◽

Vol 97 (2) ◽

pp. 239-246 ◽

Cited By ~ 17

Author(s):

Shuntaro IKEDA ◽

Mareomi HAMADA ◽

Kunio HIWADA

Keyword(s):

Heart Failure ◽

Spontaneously Hypertensive Rats ◽

Wall Stress ◽

Decompensated Heart Failure ◽

Cardiomyocyte Apoptosis ◽

Cardiac Remodelling ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Systolic Wall Stress ◽

Fractional Shortening

Various alterations in molecular and cellular events have been considered as possibly contributing to the cardiac remodelling that occurs during the transition from compensated hypertrophy to heart failure. The aim of the present study is to clarify (1) whether cardiac apoptosis occurs during the transition from compensated hypertrophy to decompensated heart failure, and (2) whether expression of the genes encoding Bax (an apoptosis inducer) and Bcl-xL and Bcl-2 (apoptosis inhibitors) is altered during this transition. We used 12-month-old and 20-month-old male spontaneously hypertensive rats (SHR12 and SHR20 respectively) and age-matched Wistar–Kyoto rats (WKY12 and WKY20 respectively). These rats were killed after measurement of haemodynamic parameters by transthoracic echocardiography and use of a tipmanometer via the right carotid artery. The expression of bcl-2, bcl-xL and bax was analysed by Northern blotting. Samples were also fixed in 4% paraformaldehyde for in situ nick end-labelling (TUNEL) methods and immunohistochemistry. SHR12 had well compensated left ventricular hypertrophy with normal fractional shortening and normal end-systolic wall stress. In contrast, the hearts of SHR20 developed decompensated dilatation, with a decrease in fractional shortening and an increase in end-systolic wall stress. TUNEL-positive cells were seen exclusively in the hearts of SHR20. The major cell types that showed TUNEL-positive nuclei were non-cardiomyocytes. The expression of bax remained unchanged during the transition to heart failure. However, there was increased expression of bcl-xL in the failing stage, whereas the expression of bcl-2 remained unchanged. Immunohistochemical studies revealed that Bcl-xL protein was up-regulated in the hearts of SHR20. In conclusion, non-cardiomyocyte apoptosis may play a contributory role in the remodelling that occurs in the transition from compensatory hypertrophy to decompensated heart failure. In addition, it is suggested that enhanced expression of bcl-xL plays an important role in the preservation of cardiomyocytes during this transition.

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Autophagic Signaling and Proteolytic Enzyme Activity in Cardiac and Skeletal Muscle of Spontaneously Hypertensive Rats following Chronic Aerobic Exercise

PLoS ONE ◽

10.1371/journal.pone.0119382 ◽

2015 ◽

Vol 10 (3) ◽

pp. e0119382 ◽

Cited By ~ 19

Author(s):

Elliott M. McMillan ◽

Marie-France Paré ◽

Brittany L. Baechler ◽

Drew A. Graham ◽

James W. E. Rush ◽

...

Keyword(s):

Skeletal Muscle ◽

Enzyme Activity ◽

Aerobic Exercise ◽

Proteolytic Enzyme ◽

Spontaneously Hypertensive Rats ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Proteolytic Enzyme Activity

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Aerobic Exercise of Low to Moderate Intensity Corrects Unequal Changes in BKCa Subunit Expression in the Mesenteric Arteries of Spontaneously Hypertensive Rats

Physiological Research ◽

10.33549/physiolres.933407 ◽

2017 ◽

pp. 219-233 ◽

Cited By ~ 4

Author(s):

Y. ZHANG ◽

Y. CHEN ◽

L. ZHANG ◽

N. LU ◽

L. SHI

Keyword(s):

Aerobic Exercise ◽

Spontaneously Hypertensive Rats ◽

Exercise Group ◽

Mesenteric Arteries ◽

Moderate Intensity ◽

Hypertensive Rats ◽

Bkca Channels ◽

Spontaneously Hypertensive ◽

Low Intensity ◽

L 14

Accumulating evidence indicates that hypertension is associated with “ion channel remodeling” of vascular smooth muscle cells (VSMCs). The objective of this study was to determine the effects of exercise intensity/volume on hypertension-associated changes in large-conductance Ca2+-activated K+ (BKCa) channels in mesenteric arteries (MAs) from spontaneously hypertensive rats (SHR). Male SHRs were randomly assigned to three groups: a low-intensity aerobic exercise group (SHR-L: 14 m/min), a moderate-intensity aerobic exercise group (SHR-M: 20 m/min), and a sedentary group (SHR). Age-matched Wistar-Kyoto rats (WKYs) were used as normotensive controls. Exercise groups completed an 8-week exercise program. Elevation of the α and β1 proteins was unequal in MA myocytes from SHRs, with the β1 subunit increasing more than the α subunit. BKCa contribution to vascular tone regulation was higher in the myocytes and arteries of SHRs compared to WKYs. SHR BKCa channel subunit protein expression, β1/α ratio, whole cell current density and single-channel open probability was also increased compared with WKYs. Aerobic exercise lowered systemic blood pressure and normalized hypertension-associated BKCa alterations to normotensive control levels in the SHRs. These effects were more pronounced in the moderate-intensity group than in the low-intensity group. There is a dose-effect for aerobic exercise training in the range of low to moderate-intensity and accompanying volume for the correction of the pathological adaptation of BKCa channels in myocytes of MAs from SHR.

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