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Effect of exercise training on Ca²⁺ release units of left ventricular myocytes of spontaneously hypertensive rats.

Carneiro-Júnior MA, Quintão-Júnior JF, Drummond LR, Lavorato VN, Drummond FR, Amadeu MA, Oliveira EM, Felix LB, Cruz JS, Mill JG, Natali AJ, Prímola-Gomes TN - Braz. J. Med. Biol. Res. (2014)

Bottom Line: Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%).Hypertension also increased the frequency of Ca²⁺ sparks (HC=7.61 ± 0.26 vs NC=4.79 ± 0.19 per 100 µm/s) and decreased its amplitude (HC=0.260 ± 0.08 vs NC=0.324 ± 0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05 ± 0.08 vs NC=1.26 ± 0.01 µm), total duration (HC=11.51 ± 0.12 vs NC=14.97 ± 0.24 ms), time to peak (HC=4.84 ± 0.06 vs NC=6.31 ± 0.14 ms), and time constant of decay (HC=8.68 ± 0.12 vs NC=10.21 ± 0.22 ms).Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, ES, Brasil.

ABSTRACT
In cardiomyocytes, calcium (Ca²⁺) release units comprise clusters of intracellular Ca²⁺ release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca²⁺ sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca²⁺ sparks (HC=7.61 ± 0.26 vs NC=4.79 ± 0.19 per 100 µm/s) and decreased its amplitude (HC=0.260 ± 0.08 vs NC=0.324 ± 0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05 ± 0.08 vs NC=1.26 ± 0.01 µm), total duration (HC=11.51 ± 0.12 vs NC=14.97 ± 0.24 ms), time to peak (HC=4.84 ± 0.06 vs NC=6.31 ± 0.14 ms), and time constant of decay (HC=8.68 ± 0.12 vs NC=10.21 ± 0.22 ms). These changes were partially reversed in HT rats (frequency of Ca²⁺ sparks=6.26 ± 0.19 µm/s, amplitude=0.282 ± 0.10 ΔF/F0, full width at half-maximum amplitude=1.14 ± 0.01 µm, total duration=13.34 ± 0.17 ms, time to peak=5.43 ± 0.08 ms, and time constant of decay=9.43 ± 0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.

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Representative images (Ai to Aiv) of spontaneous Ca2+ sparksrecorded from left ventricular isolated cardiomyocytes. NC: normotensivecontrol; HC: hypertensive control; NT: normotensive trained; HT: hypertensivetrained.
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f02: Representative images (Ai to Aiv) of spontaneous Ca2+ sparksrecorded from left ventricular isolated cardiomyocytes. NC: normotensivecontrol; HC: hypertensive control; NT: normotensive trained; HT: hypertensivetrained.

Mentions: Representative images of spontaneous Ca2+ sparks are illustrated in Figure 2 and quantified in Table 1. Cells from the HC group had a higher frequency ofspontaneous Ca2+ sparks than cells from the NC group. On the other hand,the amplitude, FWHM, FullDur, Tpeak, and τ were lower in HC than in NCcardiomyocytes. EET reduced the frequency and increased the amplitude, FWHM, FullDur,Tpeak, and τ in the NT compared with the NC group. Importantly, allalterations observed in HC group Ca2+ sparks were partially restored bythe EET program.


Effect of exercise training on Ca²⁺ release units of left ventricular myocytes of spontaneously hypertensive rats.

Carneiro-Júnior MA, Quintão-Júnior JF, Drummond LR, Lavorato VN, Drummond FR, Amadeu MA, Oliveira EM, Felix LB, Cruz JS, Mill JG, Natali AJ, Prímola-Gomes TN - Braz. J. Med. Biol. Res. (2014)

Representative images (Ai to Aiv) of spontaneous Ca2+ sparksrecorded from left ventricular isolated cardiomyocytes. NC: normotensivecontrol; HC: hypertensive control; NT: normotensive trained; HT: hypertensivetrained.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230285&req=5

f02: Representative images (Ai to Aiv) of spontaneous Ca2+ sparksrecorded from left ventricular isolated cardiomyocytes. NC: normotensivecontrol; HC: hypertensive control; NT: normotensive trained; HT: hypertensivetrained.
Mentions: Representative images of spontaneous Ca2+ sparks are illustrated in Figure 2 and quantified in Table 1. Cells from the HC group had a higher frequency ofspontaneous Ca2+ sparks than cells from the NC group. On the other hand,the amplitude, FWHM, FullDur, Tpeak, and τ were lower in HC than in NCcardiomyocytes. EET reduced the frequency and increased the amplitude, FWHM, FullDur,Tpeak, and τ in the NT compared with the NC group. Importantly, allalterations observed in HC group Ca2+ sparks were partially restored bythe EET program.

Bottom Line: Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%).Hypertension also increased the frequency of Ca²⁺ sparks (HC=7.61 ± 0.26 vs NC=4.79 ± 0.19 per 100 µm/s) and decreased its amplitude (HC=0.260 ± 0.08 vs NC=0.324 ± 0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05 ± 0.08 vs NC=1.26 ± 0.01 µm), total duration (HC=11.51 ± 0.12 vs NC=14.97 ± 0.24 ms), time to peak (HC=4.84 ± 0.06 vs NC=6.31 ± 0.14 ms), and time constant of decay (HC=8.68 ± 0.12 vs NC=10.21 ± 0.22 ms).Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, ES, Brasil.

ABSTRACT
In cardiomyocytes, calcium (Ca²⁺) release units comprise clusters of intracellular Ca²⁺ release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca²⁺ sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca²⁺ sparks (HC=7.61 ± 0.26 vs NC=4.79 ± 0.19 per 100 µm/s) and decreased its amplitude (HC=0.260 ± 0.08 vs NC=0.324 ± 0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05 ± 0.08 vs NC=1.26 ± 0.01 µm), total duration (HC=11.51 ± 0.12 vs NC=14.97 ± 0.24 ms), time to peak (HC=4.84 ± 0.06 vs NC=6.31 ± 0.14 ms), and time constant of decay (HC=8.68 ± 0.12 vs NC=10.21 ± 0.22 ms). These changes were partially reversed in HT rats (frequency of Ca²⁺ sparks=6.26 ± 0.19 µm/s, amplitude=0.282 ± 0.10 ΔF/F0, full width at half-maximum amplitude=1.14 ± 0.01 µm, total duration=13.34 ± 0.17 ms, time to peak=5.43 ± 0.08 ms, and time constant of decay=9.43 ± 0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.

Show MeSH
Related in: MedlinePlus