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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Effect of potassium on vasodilation to acetylcholine in essential hypertension.
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Effect of potassium on vasodilation to acetylcholine in essential hypertension.

机译:钾对原发性高血压患者血管舒张作用的影响。

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Patients with essential hypertension show impaired endothelium-dependent vasodilation induced by acetylcholine. Because dietary potassium supplementation increases endothelium-dependent relaxations to acetylcholine in hypertensive rats, we designed the present study to investigate whether potassium increases endothelium-dependent vasodilation in essential hypertensive patients. Therefore, in patients with essential hypertension (n = 13) and in normotensive control subjects (n = 13) we evaluated the effect of intrabrachial potassium chloride (0.2 mmol/min) on forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 micrograms/100 mL forearm tissue per minute). In both groups of patients, potassium chloride infusion augmented local plasma potassium concentrations. Furthermore, in essential hypertensive patients but not in normotensive subjects it increased the vasodilating effect of the first three infusion rates of acetylcholine. In contrast, in seven adjunctive essential hypertensive patients, potassium chloride did not alter intrabrachial sodium nitroprusside-induced forearm vasodilation (1, 2, and 4 micrograms/100 mL forearm tissue per minute). Finally, to evaluate the role of nitric oxide on potassium-dependent facilitation of acetylcholine-induced vasodilation in essential hypertension, we studied the effect of intrabrachial NG-monomethyl L-arginine (100 micrograms/100 mL per minute) in another group of seven hypertensive patients. Vasodilation to acetylcholine was again increased by potassium chloride; NG-monomethyl L-arginine slightly blunted the vasorelaxing effect of acetylcholine but abolished the potentiating effect of potassium.(ABSTRACT TRUNCATED AT 250 WORDS)
机译:原发性高血压患者表现出乙酰胆碱引起的内皮依赖性血管舒张功能受损。由于饮食中钾的补充增加了高血压大鼠对乙酰胆碱的内皮依赖性舒张作用,因此我们设计了本研究,以研究钾是否在原发性高血压患者中增加了内皮依赖性血管舒张作用。因此,在患有原发性高血压的患者(n = 13)和血压正常的对照组(n = 13)中,我们评估了肱内氯化钾(0.2 mmol / min)对肱内动脉诱发的前臂血流(应变仪体积描记)改变的影响乙酰胆碱(每分钟前臂组织0.15、0.45、1.5、4.5和15微克/ 100 mL)。在两组患者中,氯化钾输注均会增加局部血浆钾浓度。此外,在原发性高血压患者中,但在正常血压患者中则没有,它增加了乙酰胆碱的前三种输注速率的血管舒张作用。相反,在7名辅助性原发性高血压患者中,氯化钾并未改变臂内硝普钠引起的前臂血管舒张(每分钟前臂组织分别为1、2和4微克/ 100 mL)。最后,为了评估一氧化氮在原发性高血压中对乙酰胆碱诱导的血管舒张的钾依赖性促进作用中的作用,我们在另一组七个高血压患者中研究了臂内NG-单甲基L-精氨酸(100微克/ 100 mL /分钟)的作用耐心。氯化钾再次增加了血管舒张成乙酰胆碱的能力; NG-单甲基L-精氨酸使乙酰胆碱的血管松弛作用减弱,但取消了钾的增强作用。(摘要截断为250字)

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