Low-dose ouabain constricts small arteries from ouabain-hypertensive rats: implications for sustained elevation of vascular resistance.
Low-dose ouabain constricts small arteries from ouabain-hypertensive rats: implications for sustained elevation of vascular resistance.
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低剂量哇巴因收缩哇巴因高血压大鼠的小动脉：对血管阻力持续升高的影响。
DOI：
10.1152/ajpheart.00436.2009
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Blaustein,MordecaiP
中科院分区：
文献类型：
--
作者：
Zhang,Jin;Hamlyn,JohnM;Karashima,Eiji;Raina,Hema;Mauban,JosephRH;Izuka,Michelle;Berra-Romani,Roberto;Zulian,Alessandra;Wier,WGil;Blaustein,MordecaiP
对正常大鼠长期给予哇巴因会导致持续的血压（BP）升高。这种哇巴因诱导的高血压（OH）部分归因于动脉中膜胶原沉积导致三级阻力动脉（内径> 320 μm）变窄（见参考文献）。在这里，我们描述的结构和功能特性的第四阶肠系膜小动脉从控制和OH大鼠，包括低剂量哇巴因对这些动脉肌源性张力的影响。OH大鼠收缩压为138 ± 3 mmHg，对照组为124 ± 4 mmHg（P< 0.01）。加压（70 mmHg）的对照和OH动脉，只有单层肌细胞，内径均为165 μm，壁厚均为120 μm。即使在固定后，尽管血管收缩，直径和壁厚之间没有控制和OH四级动脉，而在三级动脉，这两个参数显着小于OH比对照组。生肌反应性显着增强OH四级动脉。然而，苯丙氨酸（1 μM）和高K+诱导的血管收缩和乙酰胆碱诱导的血管舒张在对照和OH动脉中相当。5 μM苯肾上腺素和10 mM咖啡因在无Ca ~（2+）培养基中引起的血管收缩表明OH动脉中可释放肌浆网Ca ~（2+）储存是正常的。重要的是，100 nM哇巴因使对照和OH动脉收缩了1026 μm，表明这种反应在OH大鼠中没有下调。哇巴因诱导的最大收缩相当于这些小动脉中流动阻力增加了约90%;因此，哇巴因在EC 50为约0.66 nM时应使阻力增加约35%。我们的结论是，动态收缩响应循环纳摩尔哇巴因在小动脉可能作出重大贡献，增加血管紧张度和血压在OH大鼠。
Prolonged ouabain administration to normal rats causes sustained blood pressure (BP) elevation. This ouabain-induced hypertension (OH) has been attributed, in part, to the narrowing of third-order resistance arteries (∼320 μm internal diameter) as a result of collagen deposition in the artery media (see Ref. ). Here we describe the structural and functional properties of fourth-order mesenteric small arteries from control and OH rats, including the effect of low-dose ouabain on myogenic tone in these arteries. Systolic BP in OH rats was 138 ± 3 versus 124 ± 4 mmHg in controls (P< 0.01). Pressurized (70 mmHg) control and OH arteries, with only a single layer of myocytes, both had ∼165-μm internal diameters and ∼20-μm wall thicknesses. Even after fixation, despite vasoconstriction, the diameters and wall thicknesses did not differ between control and OH fourth-order arteries, whereas in third-order arteries, both parameters were significantly smaller in OH than in controls. Myogenic reactivity was significantly augmented in OH fourth-order arteries. Nevertheless, phenylephrine- (1 μM) and high K+-induced vasoconstrictions and acetylcholine-induced vasodilation were comparable in control and OH arteries. Vasoconstrictions induced by 5 μM phenylephrine and by 10 mM caffeine in Ca2+-free media indicated that releasable sarcoplasmic reticulum Ca2+stores were normal in OH arteries. Importantly, 100 nM ouabain constricted both control and OH arteries by ∼26 μm, indicating that this response was not downregulated in OH rats. This maximal ouabain-induced constriction corresponds to a ∼90% increase in resistance to flow in these small arteries; thus ouabain at EC50of ∼0.66 nM should raise resistance by ∼35%. We conclude that dynamic constriction in response to circulating nanomolar ouabain in small arteries likely makes a major contribution to the increased vascular tone and BP in OH rats.
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