运动训练诱导自发性高血压大鼠生理性心脏肥大

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Abstract Objective To observe the effects of regular exercise training on cardiac hypertrophy in spontaneously hypertensive rats (SHR) and to explore the possible mechanism of exercise-induced cardioprotective effect.Methods Thirty SHRs were randomly divided into hypertension exercise group (SHR-Ex) and hypertension control group (SHR-C), and fifteen healthy Wistar rats were used as normotensive control group (NC). Rats of SHR-Ex group performed swimming training for 8 weeks (60 min per day, 5 days per week), while those of SHR-C and NC groups were kept quiet in a cage. After the experiment, the caudal artery blood pressure was measured by intelligent non-invasive blood pressure tester, the cardiac structure and function were monitored by echocardiography, the left ventricle was separated and weighed, the cross sectional area (CSA) and collagen volume fraction (CVF) of myocardial cells were obtained by HE and Masson staining respectively, and embryo genes and cardiac hypertrophy signal pathway protein expression were determined by Western Blot.Results During the experiment, a total of 7 rats were excluded due to refusal to run, death or other reasons, and finally 38 rats were included, including 15 rats in the NC group, 12 rats in the SHR-C group and 11 rats in the SHR-Ex group. Compared with NC group, SHR-C group rats showed concentric cardiac hypertrophy, myocardial fibrosis (CVF increased, P<0.05), and up-regulated expression of atrial natriuretic factor (ANF), myosin light chain-2(MLC-2), Calcineurin Aβ subunit (CNAβ), PI3 kinase p110 α subunit [PI3-K (p110α)] and phosphorylated Akt (p-Akt) . Compared with SHR-C group, SHR-Ex group showed eccentric cardiac hypertrophy, reduced myocardial fibrosis (CVF decreased, P<0.05) and enhanced cardiac function (P<0.05), the expression levels of ANF, MLC-2 and CNAβ protein expression were down-regulated (P<0.05), and PI3-K(p110α) and p-Akt had no significant change.Conclusions Long-term exercise training can promote the change from pathological cardiac hypertrophy to physiological cardiac hypertrophy in SHR, which may be related with the decline of calcineurin signal pathway activity.

Key words： exercise training spontaneously hypertensive rats cardiac hypertrophy myocardial fibrosis signal transduction pathway

Received: 20 May 2022

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	Articles by authors
	PENG Peng
	HE Ruibo
	MA Gang
	WANG Daning
	BO Hai
	QIN Yongsheng

Cite this article:

PENG Peng,HE Ruibo,MA Gang等. Effects of exercise training on physiologic cardiac hypertrophy in spontaneously hypertensive rats[J]. Med. J. Chin. Peop. Armed Poli. Forc., 2022, 33(9): 759-763.

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http://journal08.magtechjournal.com/Jwk_wjyx/EN/ OR http://journal08.magtechjournal.com/Jwk_wjyx/EN/Y2022/V33/I9/759

[1]	Fiuza-Luces C, Santos-Lozano A, Joyner M, et al. Exercise benefits in cardiovascular disease: beyond attenuation of traditional risk factors[J]. Nat Rev Cardiol, 2018, 15(12): 731-743.
[2]	Schroeder E C, Franke W D, Sharp R L, et al. Comparative effectiveness of aerobic, resistance, and combined training on cardiovascular disease risk factors: a randomized controlled trial[J]. PLoS One, 2019, 14(1): e0210292.
[3]	Emter C A, McCune S A, Sparagna G C, et al. Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats[J]. Am J Physiol Heart Circ Physiol, 2005, 289(5): H2030-2038.
[4]	O′Connor C M, Whellan D J, Lee K L, et al. Efficacy and safety of exercise training in patients with chronic heart failure: HF-ACTION randomized controlled trial[J]. JAMA, 2009, 301(14): 1439-1450.
[5]	Nakamura M, Sadoshima J. Mechanisms of physiological and pathological cardiac hypertrophy[J]. Nat Rev Cardiol, 2018, 15(7): 387-407.
[6]	Medeiros A, Oliveira E M, Gianolla R, et al. Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats[J]. Braz J Med Biol Res, 2004, 37(12): 1909-1917.
[7]	Schultz R L, Swallow J G, Waters R P, et al. Effects of excessive long-term exercise on cardiac function and myocyte remodeling in hypertensive heart failure rats[J]. Hypertension, 2007, 50(2): 410-416.
[8]	Filho A G, Ferreira A J, Santos S H, et al. Selective increase of angiotensin(1-7) and its receptor in hearts of spontaneously hypertensive rats subjected to physical training[J]. Exp Physiol, 2008, 93(5): 589-598.
[9]	Shimizu I, Minamino T. Physiological and pathological cardiac hypertrophy[J]. J Mol Cell Cardiol, 2016, 97: 245-262.
[10]	Tham Y K, Bernardo B C, Ooi J Y, et al. Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets[J]. Arch Toxicol, 2015, 89(9): 1401-1438.
[11]	McMullen J R, Jennings G L. Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure[J]. Clin Exp Pharmacol Physiol, 2007, 34(4): 255-262.
[12]	Bernardo B C, Weeks K L, Pretorius L, et al. Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies[J]. Pharmacol Ther, 2010, 128(1): 191-227.
[13]	Perrino C, Naga Prasad S V, Mao L, et al. Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction[J]. J Clin Invest, 2006, 116(6): 1547-1560.
[14]	Weeks K L, Bernardo B C, Ooi J, et al. The IGF1-PI3K-Akt signaling pathway in mediating exercise-induced cardiac hypertrophy and protection[J]. Adv Exp Med Biol, 2017, 1000: 187-210.
[15]	Gao L, Liu Y, Guo S, et al. Testin protects against cardiac hypertrophy by targeting a calcineurin-dependent signalling pathway[J]. J Cell Mol Med, 2019, 23(1): 328-339.
[16]	Liu H B, Yang B F, Dong D L. Calcineurin and electrical remodeling in pathologic cardiac hypertrophy[J]. Trends Cardiovasc Med, 2010, 20(5): 148-153.
[17]	Molkentin J D, Lu J R, Antos C L, et al. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy[J]. Cell, 1998, 93(2): 215-228.
[18]	Bueno O F, Wilkins B J, Tymitz K M, et al. Impaired cardiac hypertrophic response in Calcineurin Abeta -deficient mice[J]. Proc Natl Acad Sci U S A, 2002, 99(7): 4586-4591.
[19]	Aoyagi T, Matsui T. Phosphoinositide-3 kinase signaling in cardiac hypertrophy and heart failure[J]. Curr Pharm Des, 2011, 17(18): 1818-1824.
[20]	Dirkx E, da Costa Martins P A, de Windt L J. Regulation of fetal gene expression in heart failure[J]. Biochim Biophys Acta, 2013, 1832(12): 2414-2424.
[21]	童晓明, 孙宝珍, 高庆平. 冠心病患者血浆心钠素水平与左房功能变化的相关性分析研究[J]. 中华物理医学杂志, 1998, 20(1): 38-41.