Differential contribution of endothelial function to vascular reactivity in conduit and resistance arteries from deoxycorticosterone-salt hypertensive rats.
Differential contribution of endothelial function to vascular reactivity in conduit and resistance arteries from deoxycorticosterone-salt hypertensive rats.
复制标题
内皮功能对脱氧皮质酮盐高血压大鼠导管和阻力动脉血管反应性的差异贡献。
DOI：
10.1161/01.hyp.27.6.1245
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Davison,CB
中科院分区：
文献类型：
--
作者：
White,RM;Rivera,CO;Davison,CB
这些研究的目的是比较脱氧皮质酮盐高血压大鼠导管和阻力动脉功能的变化。我们假设，如果存在一种导致高血压血管功能变化的共同机制，那么导管动脉和阻力动脉的反应性也会发生类似的变化。准备颈总动脉的螺旋状切割条用于测量等长力的产生，并对肠系膜小动脉的片段进行加压用于视频尺寸分析。测定动脉对去氧肾上腺素和乙酰胆碱的敏感性。脱氧皮质酮盐高血压大鼠的颈动脉比对照大鼠的动脉对去氧肾上腺素更敏感，而高血压大鼠的肠系膜阻力动脉对去氧肾上腺素不太敏感。在颈动脉中，内皮剥脱或与 Nω-硝基-L-精氨酸一起孵育可将对照大鼠的去氧肾上腺素敏感性增加至脱氧皮质酮盐大鼠的水平。这些操作对脱氧皮质酮盐大鼠动脉中的去氧肾上腺素敏感性没有影响。在肠系膜阻力动脉中，内皮剥脱使高血压大鼠动脉中受抑制的去氧肾上腺素敏感性正常化，但对血压正常大鼠的动脉没有影响。脱氧皮质酮盐肠系膜动脉中去氧肾上腺素敏感性的降低并未通过与 Nω-硝基-L-精氨酸一起孵育而逆转。脱氧皮质酮盐高血压大鼠的颈动脉中乙酰胆碱诱导的舒张受到抑制，而 Nω-硝基-L-精氨酸则阻断了这些舒张。相反，正常血压和高血压大鼠肠系膜动脉中的乙酰胆碱舒张作用没有差异。Nω-硝基-L-精氨酸仅轻微但显着地减弱了高血压大鼠肠系膜阻力动脉中的乙酰胆碱扩张作用。我们得出的结论是，脱氧皮质酮盐高血压大鼠的颈动脉和肠系膜阻力动脉中血管收缩剂对去氧肾上腺素的敏感性发生了质的不同变化。在这种高血压模型中，颈动脉对去氧肾上腺素的敏感性增加是由于内皮源性一氧化氮生成的丧失。相比之下，脱氧皮质酮盐大鼠肠系膜阻力动脉中去氧肾上腺素敏感性降低是由于非一氧化氮介导的内皮细胞影响，而血压正常大鼠的动脉中不存在这种影响。
The purpose of these studies was to compare changes in conduit and resistance artery function in deoxycorticosterone-salt hypertensive rats. We hypothesized that if there was a common mechanism producing changes in vascular function in hypertension, then there would be similar alterations in reactivity of conduit and resistance arteries. Helically cut strips of common carotid artery were prepared for measurement of isometric force generation, and segments of small mesenteric arteries were pressurized for video dimension analysis. Sensitivity of arteries to phenylephrine and acetylcholine was determined. Carotid arteries from deoxycorticosterone-salt hypertensive rats were more sensitive to phenylephrine than arteries from control rats, whereas mesenteric resistance arteries from hypertensive rats were less sensitive to phenylephrine. In carotid arteries, endothelial denudation or incubation withNω-nitro-l-arginine increased phenylephrine sensitivity in control rats to the level seen in deoxycorticosterone-salt rats. These manipulations had no effect on phenylephrine sensitivity in arteries from deoxycorticosterone-salt rats. In mesenteric resistance arteries, endothelium denudation normalized the depressed phenylephrine sensitivity in arteries from hypertensive rats but had no effect on arteries from normotensive rats. This depressed phenylephrine sensitivity in deoxycorticosterone-salt mesenteric arteries was not reversed by incubation withNω-nitro-l-arginine. Acetylcholine-induced relaxation was depressed in carotid arteries from deoxycorticosterone-salt hypertensive rats, andNω-nitro-l-arginine blocked these relaxations. In contrast, acetylcholine relaxation in the mesenteric arteries from normotensive and hypertensive rats did not differ.Nω-nitro-l-arginine slightly but significantly attenuated acetylcholine dilation only in mesenteric resistance arteries from the hypertensive rats. We conclude that qualitatively different changes in vasoconstrictor sensitivity to phenylephrine occur in carotid arteries and mesenteric resistance arteries of deoxycorticosterone-salt hypertensive rats. The increased phenylephrine sensitivity in carotid arteries in this model of hypertension is due to the loss of endothelium-derived nitric oxide production. In contrast, the decreased phenylephrine sensitivity in mesenteric resistance arteries from deoxycorticosterone-salt rats is due to a non–nitric oxide–mediated influence of the endothelium that is absent in arteries from normotensive rats.