Blood pressure normalization via pharmacotherapy improves cutaneous microvascular function through NO-dependent and NO-independent mechanisms.
Blood pressure normalization via pharmacotherapy improves cutaneous microvascular function through NO-dependent and NO-independent mechanisms.
复制标题
DOI：
10.1111/micc.12382
复制
发表时间：
2017-10
期刊：
影响因子：
--
通讯作者：
Alexander LM
中科院分区：
文献类型：
--
作者：
Craighead DH;Smith CJ;Alexander LM
高血压与内皮功能障碍和血管重构有关。评估抗高血压药物治疗对皮肤微血管内皮型一氧化氮合酶和诱导型一氧化氮合酶依赖性机制和最大血管舒张能力的影响。将皮内微透析纤维放置在15名正常血压（SBP 111±2 mmHg），12名未用药的高血压（SBP 142±2 mmHg）和12名药物治疗的高血压（SBP 120±2 mmHg）受试者中。实验分为对照组、iNOS抑制组（1400 w）和NOS抑制组（L-NAME）。在局部加热（42°C）和乙酰胆碱（ACh）剂量反应方案期间测量的红细胞通量，被标准化为皮肤血管电导（CVC=通量·MAP−1）和最大血管舒张百分比（%CVCmax）。与血压正常者相比，高血压患者ACh介导的血管舒张作用减弱（p<0.001），但药物治疗受试者无此作用（p=0.83）。与高血压（p<0.001）和药物治疗（p<0.001）受试者相比，NOS抑制减弱了正常血压受试者中ACh介导的血管舒张。iNOS抑制组间乙酰胆碱介导的血管舒张无差异。与血压正常者相比，高血压患者中局部热诱导的血管舒张减弱（p<0.001），但iNOS抑制增强了高血压患者中的血管舒张，因此这种减弱被消除（p=0.31）。与血压正常者相比，高血压（p=0.014）和药物治疗受试者（p=0.004）的最大血管扩张能力降低。在皮肤微血管中，抗高血压药物治疗通过NO依赖性和非依赖性机制改善了内皮功能，但没有改善最大血管扩张能力。
Hypertension is associated with endothelial dysfunction and vascular remodeling. To assess effects of antihypertensive pharmacotherapy on eNOS and iNOS-dependent mechanisms and maximal vasodilator capacity in the cutaneous microvasculature. Intradermal microdialysis fibers were placed in 15 normotensive (SBP 111±2 mmHg), 12 unmedicated hypertensive (SBP 142±2 mmHg), and 12 medicated hypertensive (SBP 120±2 mmHg) subjects. Treatments were control, iNOS-inhibited (1400w), and NOS-inhibited (L-NAME). Red cell flux, measured during local heating (42°C) and acetylcholine (ACh) dose-response protocols, was normalized to cutaneous vascular conductance (CVC=flux•MAP−1) and a percentage of maximal vasodilation (%CVCmax). Compared to normotensives, ACh-mediated vasodilation was attenuated in the hypertensive (p<0.001), but not medicated subjects (p=0.83). NOS inhibition attenuated ACh-mediated vasodilation in normotensives compared to hypertensive (p<0.001) and medicated (p<0.001) subjects. With iNOS inhibition there was no difference in ACh-mediated vasodilation between groups. Compared to the normotensives, local heat-induced vasodilation was attenuated in the hypertensives (p<0.001), but iNOS inhibition augmented vasodilation in the hypertensives so this attenuation was abolished (p=0.31). Compared to normotensives, maximal vasodilator capacity was reduced in the hypertensive (p=0.014) and medicated subjects (p=0.004). In the cutaneous microvasculature, antihypertensive pharmacotherapy improved endothelial function through NO-dependent and independent mechanisms, but did not improve maximal vasodilator capacity.
登录
查看更多内容
影响因子：
3.3
作者：
Bruning, Rebecca S.;Santhanam, Lakshmi;Holowatz, Lacy A.
通讯作者：
Holowatz, Lacy A.
影响因子：
3.7
作者：
Gauthier, Kathryn M.;Cepura, Cody J.;Campbell, William B.
通讯作者：
Campbell, William B.
影响因子：
2.7
作者：
Fieger, Sarah M.;Wong, Brett J.
通讯作者：
Wong, Brett J.
影响因子：
5.3
作者：
Farkas, K;Kolossváry, E;Farsang, C
通讯作者：
Farsang, C
影响因子：
5
作者：
Bachetti, T;Comini, L;Ferrari, R
通讯作者：
Ferrari, R