Daily exercise-induced cardioprotection is associated with changes in calcium regulatory proteins in hypertensive rats

2005 ◽  
Vol 288 (2) ◽  
pp. H532-H540 ◽  
Author(s):  
Heidi L. Collins ◽  
Alfred M. Loka ◽  
Stephen E. DiCarlo
Keyword(s):  
Protein Expression ◽  
Epidemiological Data ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Regulatory Proteins ◽  
Hypertensive Rats ◽  
Daily Exercise ◽  
Plasmic Reticulum ◽  
Exercise Induced ◽  
Prevention Approach

Epidemiological data document that regular exercise protects against the morbidity and mortality associated with ischemic heart disease. Therefore, we tested the hypothesis that daily exercise (DE) increases the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion and alters the expression of calcium regulatory proteins. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. To test this hypothesis, we recorded the VAT in conscious sedentary normotensive, sedentary hypertensive, and DE hypertensive rats, and we associated these thresholds with the protein expression of the L-type calcium channel, Na+/Ca2+ exchanger, phospholamban, and sarco(endo)plasmic reticulum Ca2+-ATPase. Results document a significantly reduced time to ventricular arrhythmias (sedentary hypertensive, 3.7 ± 0.3 min vs. sedentary normotensive, 4.8 ± 0.3 min), an increased Na+/Ca2+ exchanger protein expression (47%), and a decreased phospholamban protein expression (−34%) in conscious hypertensive rats. DE increased the VAT (5.9 ± 0.2 min), decreased the protein expression of the Na+/Ca2+ exchanger, and normalized the protein expression of phospholamban in the hypertensive rats. Thus DE may be a primary prevention approach for reducing the incidence of arrhythmias by altering calcium regulatory proteins in hypertensive rats.

Exercise-induced activation of cardiac sympathetic nerve triggers cardioprotection via redox-sensitive activation of eNOS and upregulation of iNOS

2007 ◽  
Vol 292 (5) ◽  
pp. H2051-H2059 ◽  
Author(s):  
Yuzo Akita ◽  
Hajime Otani ◽  
Seiji Matsuhisa ◽  
Shiori Kyoi ◽  
Chiharu Enoki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery ◽  
Sympathetic Nerve ◽  
Ischemia Reperfusion ◽  
Sympathetic Nerves ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Cardiac Sympathetic Nerve ◽  
Exercise Induced ◽  
Oxide Synthase

We investigated the mechanism of exercise-induced late cardioprotection against ischemia-reperfusion (I/R) injury. C57BL/6 mice received treadmill exercise (60 min/day) for 7 days at a work rate of 60–70% maximal oxygen uptake. Exercise transiently increased oxidative stress and activated endothelial isoform of nitric oxide synthase (eNOS) during exercise and increased expression of inducible isoform of NOS (iNOS) in the heart after 7 days of exercise. The mice were subjected to regional ischemia by 30 min of occlusion of the left coronary artery, followed by 2 h of reperfusion. Infarct size was significantly smaller in the exercised mice. Ablation of cardiac sympathetic nerve by topical application of phenol abolished oxidative stress, activation of eNOS, upregulation of iNOS, and cardioprotection mediated by exercise. Treatment with the antioxidant N-(2-mercaptopropionyl)-glycine during exercise also inhibited activation of eNOS, upregulation of iNOS, and cardioprotection. In eNOS−/− mice, exercise-induced oxidative stress was conserved, but upregulation of iNOS and cardioprotection was lost. Exercise did not confer cardioprotection when the iNOS selective inhibitor 1400W was administered just before coronary artery occlusion or when iNOS−/− mice were employed. These results suggest that exercise stimulates cardiac sympathetic nerves that provoke redox-sensitive activation of eNOS, leading to upregulation of iNOS, which acts as a mediator of late cardioprotection against I/R injury.

Acute exercise increases the ventricular arrhythmia threshold via the intrinsic adenosine receptor system in conscious hypertensive rats

2005 ◽  
Vol 289 (3) ◽  
pp. H1020-H1026 ◽  
Author(s):  
Heidi L. Collins ◽  
Stephen E. DiCarlo
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmia ◽  
Adenosine Receptor ◽  
Acute Exercise ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Dynamic Exercise ◽  
Hypertensive Rats ◽  
Receptor System ◽  
Single Bout

Coronary artery occlusion-induced tachyarrhythmias that culminate in ventricular fibrillation are the leading cause of death in developed countries. The intrinsic adenosine receptor system protects the heart from an ischemic insult. Thus the increased functional demands made on the heart during exercise may produce protective adaptations mediated by endogenous adenosine. Therefore, we tested the hypothesis that a single bout of dynamic exercise increases the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion in conscious hypertensive rats via the intrinsic adenosine receptor system. To test this hypothesis, we recorded the VAT before and on an alternate day after a single bout of dynamic treadmill exercise (12 m/min, 10% grade for 40 min). A single bout of dynamic exercise significantly reduced postexercise arterial pressure (Δ−24 ± 4 mmHg) and increased VAT (Δ+1.95 ± 0.31 min). Adenosine receptor blockade with the nonselective adenosine receptor antagonists theophylline or aminophylline (10 mg/kg) attenuated the cardioprotective effects of a single bout of dynamic exercise. Results suggest that strategies that increase myocardial ATP requirements leading to adenosine production provide protection against coronary artery occlusion.

scholarly journals Exercise-Induced Spastic Coronary Artery Occlusion at the Site of a Moderate Stenosis

Circulation ◽  
2010 ◽  
Vol 122 (23) ◽  
Author(s):  
Ali Yilmaz ◽  
Stephan Hill ◽  
Tim Schäufele ◽  
Matthias Vöhringer ◽  
Angela Geissler ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Exercise Induced

Sarcolemmal permeability changes during early myocardial anoxia

1978 ◽  
Vol 36 (2) ◽  
pp. 642-643
Author(s):  
M. Ashraf ◽  
L. Landa ◽  
L. Nimmo ◽  
C. M. Bloor
Keyword(s):  
Cell Membrane ◽  
Membrane Permeability ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Cell Membrane Permeability ◽  
Enzyme Release ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Sarcolemmal Permeability ◽  
Membrane Changes

Following coronary artery occlusion, the myocardial cells lose intracellular enzymes that appear in the serum 3 hrs later. By this time the cells in the ischemic zone have already undergone irreversible changes, and the cell membrane permeability is variably altered in the ischemic cells. At certain stages or intervals the cell membrane changes, allowing release of cytoplasmic enzymes. To correlate the changes in cell membrane permeability with the enzyme release, we used colloidal lanthanum (La+++) as a histological permeability marker in the isolated perfused hearts. The hearts removed from sprague-Dawley rats were perfused with standard Krebs-Henseleit medium gassed with 95% O2 + 5% CO2. The hypoxic medium contained mannitol instead of dextrose and was bubbled with 95% N2 + 5% CO2. The final osmolarity of the medium was 295 M osmol, pH 7. 4.

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