Hypertension

Feihl, François; Liaudet, Lucas; Waeber, Bernard; Lévy, Bernard

doi:10.1161/01.hyp.0000249510.20326.72

Cited by 219 publications

(107 citation statements)

References 107 publications

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“…Imbalance in vascular tonus control observed in microcirculation in hypertension may be the result of excessive vasoconstriction causing occlusion of resistance arterioles and non-perfusion of capillaries, inducing microvascular rarefaction and decrease of conductibility in parallel to skeletal muscular microcirculation [3][4][5][6] . Furthermore, studies have shown that the endothelial shear stress leads to sustained release of endothelial nitric oxide synthase (eNOS) and the absence of blood flow, and of NO as well, could lead to endothelial dysfunction followed by peripheral apoptosis and later on, loss of non-perfused vessels in hypertension, promoting hence the microvascular rarefaction scenario.…”

Section: Discussionmentioning

confidence: 99%

“…Normal cardiac output followed by increase of peripheral vascular resistance are considered the most remarkable marks of hypertension essential in adults, demonstrating that high BP is associated with damage in microcirculation 3,4 . Considerable data show that microvascular abnormalities such as reduction of blood flow and microvascular rarefaction are clear evidence of the disturb in the angiogenic process and greater destruction of vessels in hypertension [3][4][5][6] . Many factors have been pointed as responsible for the endothelial dysfunction and by fail in the angiogenic process in hypertension.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, aerobic exercise normalizes peripheral vascular resistance for the skeletal musculature and the arterial wall-to-lumen ratio 17 . Restoration of the microvascular chain may importantly contribute to the decrease in BP through reduction in peripheral vascular resistance, which has been said to be responsible for hypertension in adults 3,4,[17][18][19] . Increase in blood flow to the skeletal musculature promoted by aerobic ET and consequent increase of shear stress present direct correlation with increase in release of NO and VEGF, which also contributes to flow increase, since it leads not only to endothelium--dependent vasodilatation but also to angiogenesis, being considered by many researchers the primary sign for vascular remodeling 20 .…”

Section: Introductionmentioning

confidence: 99%

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O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

Fernandes

Magalhães

Carmo

et al. 2012

Rev Bras Med Esporte

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Aerobic exercise training (ET) has been established as an important non-pharmacological treatment for hypertension, since it corrects the microvascular rarefaction and decreases blood pressure. Studies have shown that microvascular abnormalities are directly associated with changes in the vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2), as well as with imbalance of apoptotic signaling in hypertension. However, little is known about these mechanisms in hypertension. We hypothesized that ET restores angiogenic factors and promotes balance between anti and pro-apoptotic proteins of the Bcl-2 family, potentially contributing to revascularization and the disease regression. Twelve-week old male Spontaneously Hypertensive Rats (SHR, n=14) and Wistar Kyoto Rats (WKY, n=14) were randomly assigned into 4 groups: SHR, trained SHR (SHR-T), WKY and trained WKY (WKY-T) were studied. As expected, ten weeks of ET were effective in reducing blood pressure in SHR-T group. In addition, ET promoted resting bradycardia in trained groups (WKY-T and SHR-T), being considered an important marker of aerobic ET. ET has also corrected the capillary rarefaction in SHR-T and this response is partly due to recovery of the peripheral levels of VEGF and increase in VEGFR2 expression. Concomitantly, normalization of the apoptotic pathway was observed, with increased expression of the anti-apoptotic proteins (Bcl-2 and Bcl-x) and reduction of the pro-apoptotic protein (Bad), followed by phosphorylation of the Bad protein and decrease in the Bad/Bcl-x association. These data suggest that ET promotes peripheral revascularization in hypertension dependent on a fine balance between positive and negative regulators of angiogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

Fernandes

Magalhães

Carmo

et al. 2012

Rev Bras Med Esporte

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“…Animal studies have provided evidence to support these hypotheses (for extended reviews, see Skov and Mulvany, 29 Intengan and Schiffrin, 30 Feihl et al 31 ). Hemodynamic studies indicated that increased renal vascular resistance is already present in the prehypertensive state in SHR.…”

Section: Role Of the Renal Microvascular Remodeling In The Pathogenesmentioning

confidence: 99%

Prevention and regression of hypertension: role of renal microvascular protection

et al. 2009

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Hypertension is a disease which affects over 26.4% of the world adult population, therefore novel approaches to the prevention and treatment of this disease need to be examined. Previous studies from our and other laboratories have shown that treatment of spontaneously hypertensive rats (SHR) and Dahl salt-sensitive rats with a renin-angiotensin system (RAS) inhibitor during the 'critical period' in hypertension development results in prevention of the later development of hypertension. In humans, Julius et al. reported similar findings in the landmark TROPHY study. Recently, we reported that 'pulse' treatment of SHR with highdose angiotensin receptor blocker (ARB) is effective in causing sustained reduction of already established hypertension, even when the treatment was started after the 'critical period'. These results suggest the possibility that 'regression' of established hypertension may become feasible, and we have started a prospective, multicenter clinical study (STAR CAST study) to examine this possibility. In our animal studies, we found that treatment of rats during the 'critical period' with an ARB inhibits the development of renal arteriolar hypertrophy. Moreover, a high-dose angiotensin blocker caused a remarkable reversal of renal arteriolar hypertrophy in SHR, which was associated with changes in microvascular MMP expression. These results suggest that changes in the renal microvasculature may have an important role in the mechanisms of hypertension prevention and regression by ARB.

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“…[8][9][10][11] The microcirculation is generally defined as the network of small arteries, arterioles capillaries and venules that serve metabolic and other tissues. [12][13][14] Microcirculatory dysfunction has been proposed to be an additional mechanism relating obesity to CVD, through insulin resistance and hypertension. 15 Reduced capillary blood flow may contribute to the development of insulin resistance in muscle and other organs.…”

Section: Introductionmentioning

confidence: 99%

Macrovascular and microvascular dysfunction in the metabolic syndrome

et al. 2010

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The metabolic syndrome (MetS) is associated with increased risk of type-2 diabetes and cardiovascular disease (CVD). We hypothesized that both small and large arteries may be impaired in subjects with the MetS, even in the absence of known CVD or diabetes. We compared both skin capillary density (CD) and pulse-wave velocity (PWV) in 36 cases with the MetS with those from 108 age-and gender-matched controls from the SU.VIM.AX-2 cohort. Compared with controls, MetS subjects demonstrated increased PWV (12.2 ± 2.8 vs. 10.7 ± 1.9 m s À1 , P¼0.005) and lower functional CD (83.1 ± 15.7 vs. 89.4 ± 14.2 capillaries per mm 2 , P¼0.03). Functional CD was inversely related to fasting glucose, triglycerides (TGs) and HOMA-IR (all Po0.05). On the other hand, no association was found between CD and BP or with PWV. In multivariate models, the odds ratios (95% confidence interval) for one standard deviation change, for having an impaired PWV (X12 m s À1 , n¼44), were: 1.65 (1.11-2.45) for systolic BP and 1.93 (1.25-2.99) for TG only. For impaired CD (p80 capillaries per mm 2 ), the odds ratios (95% confidence interval) were 1.45 (1.00-2.08) for TG and 1.65 (1.13-2.43) for fasting glucose, only. In conclusion, MetS subjects exhibited evidence of macro-and microcirculatory dysfunction, even in the absence of diabetes and CVD. The common mechanism linking MetS components to CVD risk through small-and large-artery dysfunctions may be mediated through metabolic factors related to insulin resistance, not to increased BP.

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Hypertension

Cited by 219 publications

References 107 publications

O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

Prevention and regression of hypertension: role of renal microvascular protection

Macrovascular and microvascular dysfunction in the metabolic syndrome

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