Moderate exercise training does not worsen left ventricle remodeling and function in untreated severe hypertensive rats

Boissière, Julien; Eder, Véronique; Machet, Marie‐Christine; Courteix, Daniel; Bonnet, Pierre

doi:10.1152/japplphysiol.00442.2007

Cited by 31 publications

(33 citation statements)

References 30 publications

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“…In the present study, ANG-(1-7) infusion did not show any effect on LV functions. In fact, the 2K1C hypertensive model may not be appropriate to evaluate the effect of ANG-(1-7) on LV functions as cardiac functions were intact in 2K1C rats as observed by us and other studies (4,53).…”

Section: Discussionmentioning

confidence: 82%

“…THE NEWLY DISCOVERED renin-angiotensin system (RAS) axisangiotensin-converting enzyme 2 (ACE2)/angiotensin- (1)(2)(3)(4)(5)(6)(7) [ANG-(1-7)]/Mas receptor, coined as a counteregulatory axis to ACE/ANG II/angiotensin type 1 receptor (AT 1 R), is considered as an important core factor in cardiovascular pathophysiology (8,16). ACE2 metabolizes ANG II into ANG-(1-7), one of the major pathways for ANG-(1-7) production among others (8,11,16,19).…”

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confidence: 99%

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Angiotensin-(1–7) attenuates hypertension in exercise-trained renal hypertensive rats

Shah

Lee

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Shah A, Oh YB, Lee SH, Lim JM, Kim SH. Angiotensin-(1-7) attenuates hypertension in exercise-trained renal hypertensive rats. Am J Physiol Heart Circ Physiol 302: H2372-H2380, 2012. First published March 30, 2012 doi:10.1152 doi:10. /ajpheart.00846.2011 [ANG-(1-7)] plays a counterregulatory role to angiotensin II in the renin-angiotensin system. In trained spontaneous hypertensive rats, Mas expression and protein are upregulated in ventricular tissue. Therefore, we examined the role of ANG-(1-7) on cardiac hemodynamics, cardiac functions, and cardiac remodeling in trained two-kidney one-clip hypertensive (2K1C) rats. For this purpose, rats were divided into sedentary and trained groups. Each group consists of sham and 2K1C rats with and without ANG-(1-7) infusion. Swimming training was performed for 1 h/day, 5 days/wk for 4 wk following 1 wk of swimming training for acclimatization. 2K1C rats showed moderate hypertension and left ventricular hypertrophy without changing left ventricular function. Chronic infusion of ANG-(1-7) attenuated hypertension and cardiac hypertrophy only in trained 2K1C rats but not in sedentary 2K1C rats. Chronic ANG-(1-7) treatment significantly attenuated increases in myocyte diameter and cardiac fibrosis induced by hypertension in only trained 2K1C rats. The Mas receptor, ANG II type 2 receptor protein, and endothelial nitric oxide synthase phosphorylation in ventricles were upregulated in trained 2K1C rats. In conclusion, chronic infusion of ANG-(1-7) attenuates hypertension in trained 2K1C rats. swimming exercise training; atrial natriuretic peptide; cardiac hypertrophy; Mas receptor THE NEWLY DISCOVERED renin-angiotensin system (RAS) axisangiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [ANG-(1-7)]/Mas receptor, coined as a counteregulatory axis to ACE/ANG II/angiotensin type 1 receptor (AT 1 R), is considered as an important core factor in cardiovascular pathophysiology (8, 16). ACE2 metabolizes ANG II into ANG-(1-7), one of the major pathways for ANG-(1-7) production among others (8,11,16,19). The action of ANG-(1-7) includes vasorelaxation (46, 49), antihypertension (48, 55), antihypertrophy (25,36,52), and antifibrosis (20, 25), which are opposite to ANG II actions. At the receptor level, Mas receptor can hetero-oligomerize with AT 1 R and by so doing inhibit the actions of ANG II (31). Chronic or acute infusion of ANG-(1-7) has been shown to decrease blood pressure (BP) in spontaneously hypertensive rats (SHR; Refs. 2, 40) and high fructose diet-fed rats (20). Chronic infusion of Mas receptor antagonist or treatment with the ACE2 inhibitor worsens the course of hypertension accompanied with a decreased renal hemodynamics (5). Both Mas receptor and ACE2 knockout animals show an impaired cardiac function (22,50,55), and cardiovascular symptoms during cardiovascular pathophysiology are more aggravated in these animals (7,28,44). In contrast, ANG-(1-7) does not prevent hypertension induced by ANG II infusion (9, 21) and in two-kidney, one-clipped (2K1C) hypertension (5). Th...

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Section: Discussionmentioning

confidence: 82%

mentioning

confidence: 99%

Angiotensin-(1–7) attenuates hypertension in exercise-trained renal hypertensive rats

Shah

Lee

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…These alterations increase flow and O 2 extraction, as well as improving the autonomic control of the circulation. [1][2][3][4][5][6] The renin-angiotensin-aldosterone system (RAS) is a widely distributed regulatory system, with hormonal and intacrine functions in many tissues. [7][8][9][10] Angiotensin II (AngII) plays an important role in the control of water electrolyte and blood pressure.…”

Section: Introductionmentioning

confidence: 99%

Long-term exercise attenuates blood pressure responsiveness and modulates kidney angiotensin II signalling and urinary sodium excretion in SHR

Ciampone

Borges

Lima

et al. 2011

J Renin Angiotensin Aldosterone Syst

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Observations have been made regarding the effects of long-term exercise training on blood pressure, renal sodium handling and renal renin-angiotensin-aldosterone (RAS) intracellular pathways in conscious, trained Okamoto-Aoki spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKy) normotensive rats, compared with appropriate agematched sedentary SHR and WKy. To evaluate the influence of exercise training on renal function and RAS, receptors and intracellular angiotensin II (AngII) pathway compounds were used respectively, and lithium clearance and western blot methods were utilised. The current study demonstrated that increased blood pressure in SHR was blunted and significantly reduced by long-term swim training between the ages of 6 and 16 weeks. Additionally, the investigators observed an increased fractional urinary sodium excretion in trained SHR (SHR T ) rats, compared with sedentary SHR (SHR S ), despite a significantly decreased creatinine clearance (C Cr ). Furthermore, immunoblotting analysis demonstrated a decreased expression of AT1 R in the entire kidney of T SHR rats, compared with S SHR . Conversely, the expression of the AT2 R , in both sedentary and trained SHR, was unchanged. The present study may indicate that, in the kidney, long-term exercise exerts a modulating effect on AngII receptor expression. In fact, the present study indicates an association of increasing natriuresis, reciprocal changes in renal AngII receptors and intracellular pathway proteins with the fall in blood pressure levels observed in T SHR rats compared with age-matched S SHR rats.

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“…Rakusan et al (56) underwent the mouse will 2K1C a swimming protocol with moderate intensity for only 6 weeks and did not observe BP reduction after training. Boissier et al (57) used 70% of maximum effort achieved on a treadmill for mice to prescribe 10 weeks of APT and did not obtain attenuation of hypertension in this model. However, it is important to note that there was a decrease in pulse pressure in two of the studies cited above, which could be associated will decrease in arterial stiffness, suggesting that APT may improve vascular compliance in this experimental model.…”

Section: Renovascular Hypertensionmentioning

confidence: 94%

“…However, it is important to note that there was a decrease in pulse pressure in two of the studies cited above, which could be associated will decrease in arterial stiffness, suggesting that APT may improve vascular compliance in this experimental model. (55,57) Whereas Ang (1-7) presents a counter-regulatory role for angiotensin II in RAS, Shah et al (58) recently Demonstrated que the swimming TFA carried out for 4 weeks by 2K1C animals treated with Ang (1-7) to attenuated hypertension and cardiac hypertrophy evidenced by the smaller diameter of myocytes and fibrosis in the trained animals.…”

Section: Renovascular Hypertensionmentioning

confidence: 99%

Effects of aerobic exercise training in animal models of hypertension.

Palma¹,

Malfitano²,

Shimojo³

et al. 2015

mtprehabjournal

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Background: Hypertension is one of the leading causes of death due to stroke, heart attack and kidney failure. The understanding of the pathophysiological mechanisms involved in its development and maintenance is critical to potential therapeutic interventions. Thus, animal models of hypertension have been used in the study of this disease for many years. Objective: To investigated the effects of dynamic aerobic exercise training as a non-pharmacological approach for the management of hypertension in animal models. Method/Design: This study is a literature review conducted in the Medline database. Results: The results demonstrated that aerobic exercise training may reduce blood pressure in different rat models of hypertension. Conclusions: The dynamic aerobic exercise can reduced blood pressure in different animal models of hypertension by mechanisms that involving neurohumoral changes, reinforcing the important role of this approach in the treatment of hypertension and its associated disorders.

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Moderate exercise training does not worsen left ventricle remodeling and function in untreated severe hypertensive rats

Cited by 31 publications

References 30 publications

Angiotensin-(1–7) attenuates hypertension in exercise-trained renal hypertensive rats

Angiotensin-(1–7) attenuates hypertension in exercise-trained renal hypertensive rats

Long-term exercise attenuates blood pressure responsiveness and modulates kidney angiotensin II signalling and urinary sodium excretion in SHR

Effects of aerobic exercise training in animal models of hypertension.

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