Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Aug;111(2):172-179.
doi: 10.5935/abc.20180113. Epub 2018 Jul 2.

Physical Exercise and Regulation of Intracellular Calcium in Cardiomyocytes of Hypertensive Rats

[Article in English, Portuguese]
Affiliations

Physical Exercise and Regulation of Intracellular Calcium in Cardiomyocytes of Hypertensive Rats

[Article in English, Portuguese]
Joel Alves Rodrigues et al. Arq Bras Cardiol. 2018 Aug.

Abstract

Background: Regulation of intracellular calcium (Ca2+) in cardiomyocytes is altered by hypertension; and aerobic exercise brings benefits to hypertensive individuals.

Objective: To verify the effects of aerobic exercise training on contractility and intracellular calcium (Ca2+) transients of cardiomyocytes and on the expression of microRNA 214 (miR-214) in the left ventricle of spontaneously hypertensive rats (SHR).

Methods: SHR and normotensive Wistar rats of 16 weeks were divided into 4 groups -sedentary hypertensive (SH); trained hypertensive (TH); sedentary normotensive (SN); and trained normotensive (TN). Animals of the TH and TN groups were subjected to treadmill running program, 5 days/week, 1 hour/day at 60-70% of maximum running velocity for 8 weeks. We adopted a p ≤ 0.05 as significance level for all comparisons.

Results: Exercise training reduced systolic arterial pressure in hypertensive rats. In normotensive rats, exercise training reduced the time to 50% cell relaxation and the time to peak contraction and increased the time to 50% decay of the intracellular Ca2+ transients. In SHR, exercise increased the amplitude and reduced the time to 50% decay of Ca2+ transients. Exercise training increased the expression of miR-214 in hypertensive rats only.

Conclusion: The aerobic training applied in this study increased the availability of intracellular Ca2+ and accelerated the sequestration of these ions in left ventricular myocytes of hypertensive rats, despite increased expression of miR-214 and maintenance of cell contractility.

PubMed Disclaimer

Conflict of interest statement

Potential Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Figures

Figure 1
Figure 1
(A) Time to exhaustion of normotensive and hypertensive before (pre) and after (post) training. (B) Running velocity during training sessions. TN: trained normotensive; TH: trained hypertensive. Data are expressed as mean ± SD of 8 animals in each group. * compared with TN (pre); # compared with TH (pre) (p < 0.05).
Figure 2
Figure 2
Systolic arterial pressure (SAP) in normotensive animals and hypertensive animals. (A) SAP pre-training vs. post-training). (B) Final SAP of the groups. SN: sedentary normotensive; TN: trained normotensive; SH: sedentary hypertensive; TH: trained hypertensive. Data are expressed as mean ± SD of 8 animals in each group. * compared with TN (pre) (A) SN (B); & compared with TN (post) (A) TN (B); # compared with TH (pre) (A) SN (B); * compared with TH-post (A) TH (B) (p < 0.05).
Figure 3
Figure 3
Cardiomyocyte contractility in normotensive and hypertensive animals. (A) Contraction amplitude expressed as percentage of change in cell length at rest (%c.l.r.) after electrical stimulation at 1HZ; (B) time to peak concentration; (C) time to 50% of relaxation; SN, sedentary normotensive; TN, trained normotensive; SH, sedentary hypertensive; TH, trained hypertensive. Data as mean ± SD of 60-80 cells in each group. * compared with SN; # compared with SN; + compared with TH (p < 0.05).
Figure 4
Figure 4
Intracellular Ca2+ transient levels in cardiomyocytes of normotensive and hypertensive animals. (A) Amplitude of intracellular calcium. (B) Time to peak intracellular calcium. (C) Time to 50% decay of intracellular calcium. SN, sedentary normotensive; TN, trained normotensive; SH, sedentary hypertensive; TH, trained hypertensive. Data as mean ± SD of 40-50 cells in each group. * compared with SN; & compared with TN; # compared with SN; + compared with TH (p < 0.05).
Figure 5
Figure 5
MicroRNA-214 expression in the left ventricle in normotensive and hypertensive animals. SN: sedentary normotensive; TN: trained normotensive; SH: sedentary hypertensive; TH: trained hypertensive. Data as mean ± SD of 5 animals in each group. * compared with SN; & compared with TN; # compared with SN (p < 0.05).

Comment in

References

    1. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Fibrosis and renin-angiotensin-aldosterone system. Circulation. 1991;83(6):1849–1865. - PubMed
    1. Díez J, Querejeta R, López B, González A, Larman M, Martínez Ubago JL. Losartan-dependent regression of myocardial fibrosis is associated with reduction of left ventricular chamber stiffness in hypertensive patients. Circulation. 2002;105(21):2512–2517. - PubMed
    1. Miguel-Carrasco JL, Zambrano S, Blanca AJ, Mate A, Vázquez CM. Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB. J Inflamm (Lond) 2010;7:21–21. - PMC - PubMed
    1. Huang CY, Yang AL, Lin YM, Wu FN, Lin JA, Chan YS, et al. Anti-apoptotic and pro-survival effects of exercise training on hypertensive hearts. J Appl Physiology (1985) 2012;112(5):883–891. - PubMed
    1. Pescatello LS, Franklin BA, Fagard R, Farquhar WB, Kelley GA, Ray CA, et al. American College of Sports Medicine American College of Sports Medicine position stand. Exercise and hypertension. Med Sci Sports Exerc. 2004;36(3):533–553. - PubMed