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缬沙坦对高盐饮食下自发性高血压大鼠颈动脉力学性能的影响。

Effects of valsartan on mechanical properties of the carotid artery in spontaneously hypertensive rats under high-salt diet.

作者信息

Labat C, Lacolley P, Lajemi M, de Gasparo M, Safar M E, Benetos A

机构信息

INSERM U337, Paris, France.

出版信息

Hypertension. 2001 Sep;38(3):439-43. doi: 10.1161/01.hyp.38.3.439.

DOI:10.1161/01.hyp.38.3.439
PMID:11566919
Abstract

The aim of this investigation was to evaluate the influence of a high-salt diet (HSD) on the effects of valsartan, an angiotensin II type 1 (AT(1)) receptor antagonist, on carotid arterial stiffness and structure in spontaneous hypertensive rats (SHR). Carotid arterial stiffness was studied in SHR receiving a HSD or a normal-salt diet (NSD) from the 10th to 20th week of age. Within each of the 2 groups, the animals received treatment with either placebo or valsartan (30 mg. kg(-1). d(-1)) administered on the 4th to 20th week of age. Arterial pressure, wall stress, incremental elastic modulus (Einc), medial cross-sectional area, and EIIIA fibronectin isoform were significantly increased in placebo-HSD rats compared with placebo-NSD rats with no change in the ratio of collagen to elastin. Valsartan reduced mean arterial pressure in both NSD and HSD rats but reduced pulse pressure only in NSD rats. In NSD rats, valsartan reduced Einc and medial cross-sectional area. In HSD, valsartan increased Einc and did not modify medial cross-sectional area and fibronectin. In valsartan-treated rats, the ratio of collagen to elastin was greater in HSD than in NSD rats. In conclusion, the effects of AT(1) blockade are greatly influenced by salt intake in SHR. Despite a reduction in mean arterial pressure in HSD rats, AT(1) blockade was not able to prevent the effects of a HSD on pulse pressure, carotid artery stiffness, and hypertrophy.

摘要

本研究的目的是评估高盐饮食(HSD)对缬沙坦(一种血管紧张素II 1型(AT(1))受体拮抗剂)对自发性高血压大鼠(SHR)颈动脉僵硬度和结构的影响。在10至20周龄的SHR中研究了接受HSD或正常盐饮食(NSD)的大鼠的颈动脉僵硬度。在这两组中的每组内,动物在4至20周龄时接受安慰剂或缬沙坦(30 mg·kg(-1)·d(-1))治疗。与安慰剂-NSD大鼠相比,安慰剂-HSD大鼠的动脉压、壁应力、增量弹性模量(Einc)、中膜横截面积和EIIIA纤连蛋白亚型显著增加,而胶原蛋白与弹性蛋白的比例没有变化。缬沙坦降低了NSD和HSD大鼠的平均动脉压,但仅降低了NSD大鼠的脉压。在NSD大鼠中,缬沙坦降低了Einc和中膜横截面积。在HSD大鼠中,缬沙坦增加了Einc,且未改变中膜横截面积和纤连蛋白。在接受缬沙坦治疗的大鼠中,HSD大鼠的胶原蛋白与弹性蛋白的比例高于NSD大鼠。总之,AT(1)受体阻断的作用在SHR中受盐摄入的影响很大。尽管HSD大鼠的平均动脉压降低,但AT(1)受体阻断并不能预防HSD对脉压、颈动脉僵硬度和肥厚的影响。

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