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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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Gene expression of (A) RyR2 and(B) FKBP12.6 in left ventricles. NC:normotensive control; HC: hypertensive control; NT: normotensive trained; HT:hypertensive trained. Data are reported as means±SE of 5-6 animals in eachgroup. *P<0.05, compared to NC; #P<0.05, compared to HC;+P<0.05, compared to NT (two-way ANOVA followed by thepost hoc Tukey test).
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f01: Gene expression of (A) RyR2 and(B) FKBP12.6 in left ventricles. NC:normotensive control; HC: hypertensive control; NT: normotensive trained; HT:hypertensive trained. Data are reported as means±SE of 5-6 animals in eachgroup. *P<0.05, compared to NC; #P<0.05, compared to HC;+P<0.05, compared to NT (two-way ANOVA followed by thepost hoc Tukey test).

Mentions: As shown in Figure 1A and B, hypertensionresulted in a significant 270% increase in RyR2 gene expression inthe HC group compared with the NC group. Similarly, EET significantly increasedRyR2 expression by 280% in the NT group. In the HT group, EETrestored RyR2 expression to levels similar to those in the NC group.Regarding FKBP12.6, there was significantly lower expression in theHC group (88%) than in the NC group. Despite the fact that EET did not modifyFKBP12.6 response in the NT group, EET normalizedFKBP12.6 gene expression in the HT group.


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)

Gene expression of (A) RyR2 and(B) FKBP12.6 in left ventricles. NC:normotensive control; HC: hypertensive control; NT: normotensive trained; HT:hypertensive trained. Data are reported as means±SE of 5-6 animals in eachgroup. *P<0.05, compared to NC; #P<0.05, compared to HC;+P<0.05, compared to NT (two-way ANOVA followed by thepost hoc Tukey test).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f01: Gene expression of (A) RyR2 and(B) FKBP12.6 in left ventricles. NC:normotensive control; HC: hypertensive control; NT: normotensive trained; HT:hypertensive trained. Data are reported as means±SE of 5-6 animals in eachgroup. *P<0.05, compared to NC; #P<0.05, compared to HC;+P<0.05, compared to NT (two-way ANOVA followed by thepost hoc Tukey test).
Mentions: As shown in Figure 1A and B, hypertensionresulted in a significant 270% increase in RyR2 gene expression inthe HC group compared with the NC group. Similarly, EET significantly increasedRyR2 expression by 280% in the NT group. In the HT group, EETrestored RyR2 expression to levels similar to those in the NC group.Regarding FKBP12.6, there was significantly lower expression in theHC group (88%) than in the NC group. Despite the fact that EET did not modifyFKBP12.6 response in the NT group, EET normalizedFKBP12.6 gene expression in the HT group.

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