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.
Highlights
In cardiomyocytes, calcium release units (CRUs) refer to clusters of intracellular Ca2+ channels located on the sarcoplasmic membrane (SR) [1]
General characteristics and physical capacity It is important to note that spontaneously hypertensive rat (SHR) presented with increased (P,0.05) ventricular hypertrophy index, i.e., elevated ventricular weight to body weight ratio (VW/BW, hypertensive control (HC)=4.68±0.12 vs NC=4.03±0.25 mg/g) and left ventricular weight to body weight ratio (LVW/BW, HC= 3.60±0.16 vs NC=3.18±0.19 mg/g)
ryanodine receptor type 2 (RyR2) and FKBP12.6 gene expression As shown in Figure 1A and B, hypertension resulted in a significant 270% increase in RyR2 gene expression in the HC group compared with the NC group
Summary
Calcium release units (CRUs) refer to clusters of intracellular Ca2+ channels located on the sarcoplasmic membrane (SR) [1]. Release channels are known as RyR2 and are largely arranged in supramolecular arrays (10-300 RyR2) separated from the sarcolemmal membrane by a dyadic subspace of ,15 nm. Local Ca2+ elevations resulting from the synchronized opening of RyR2 are defined as calcium sparks. The normal functioning of CRUs is essential to local control of Ca2+ release during excitation-contraction coupling (ECC) [2] and is influenced by several factors including tight junction protein-protein.
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