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Exercise Training Restores Hypertension-Induced Changes in the Elastic Tissue of the Thoracic Aorta

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JOURNAL OF VASCULAR RESEARCH
卷 48, 期 6, 页码 513-524

出版社

KARGER
DOI: 10.1159/000329590

关键词

Thoracic aorta; Vascular remodelling; Elastic fibres; Smooth muscle cells; Collagen; Gene expression; Spontaneously hypertensive rats; Exercise training

资金

  1. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [06/50548-9, 08/53961-0]
  2. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - CAPES
  3. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)

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Background/Aims: Pharmacological antihypertensive therapies decrease both wall hypertrophy and collagen, but are unable to diminish the elastic content in the thoracic aorta. We investigated the effects of exercise training on aortic structure and function. Methods: Spontaneously hypertensive rats (SHR) and normotensive rats (WKY), submitted to low-intensity training (T) or kept sedentary (S), were subjected to haemodynamic analyses. The thoracic aorta was processed for real-time PCR, light (morphometric/stereological evaluations) and electron microscopy. Results: SHR S versus WKY S exhibited a higher heart rate, pressure and pulse pressure, increased alpha-actin, elastin and collagen mRNA expression, augmented wall volume and cross-sectional area (marked elastin/collagen content). In the SHR, training reduced pressure and heart rate, with slight reduction in pulse pressure. SHR T aortas exhibited small morphometric changes, reduced alpha-actin, elastin and collagen mRNA expression, normalization of increased elastic content, reduction in collagen/connective tissue and a decrease in smooth muscle cell volume (p < 0.05 for all comparisons). SHRT aortas showed improved circumferential orientation of smooth muscle cells and prevention of rupture/duplication of internal elastic lamina. No effects were observed in trained WKY aortas. Conclusions: Training effectively corrects elastic, collagen and smooth muscle content in SHR aortas. These changes, by reducing aortic pulsatility, facilitate a buffering function and reduce the cardiovascular risk. Copyright (C) 2011 S. Karger AG, Basel

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