血管紧张的

In addition, plasma angiotensin II causes the release of aldosterone in the renin-angiotensin-aldosterone system.

此外，血浆血管紧张素Ⅱ导致醛固酮释放的肾素血管紧张素醛固酮系统。

The blood pressure of.1 of pathology physiology mechanism that SAS causes CVD breathes time-out to be able to bring about airframe in elevatory Morpheus anoxic, sympathetic is excessive and excited, element of serous catechu phenolic amine, kidney and hemal endodermis element are elevatory, bring about hemal easy of hemal convulsion; to shrink the function is disorder, can make blood-vessel flowing flesh happening reframes and fleshy, systemic blood-vessel obstruction adds element of the kidney when; is chronic and anoxic, system of hemal and nervous element is activationed, bring about blood pressure to lift. Obstruction of way of energy of life of patient of OSAS of disease of blood of 1.2 low oxygen increases, cause air current to interrupt, breath pauses, at the same time airframe gets used to low oxygen environment gradually, breathing centre drops to low oxygen and sensitivity of disease of blood of tall carbonic acid, breath suspends a frequency increasing, farther aggravating airframe is anoxic. 1.3 heads are self-adjusting the function drops normal person changes quickly in systematic circulation blood pressure when, the head can be passed adjust independently functional generation protects effect, make change of cerebral blood flow not big.

SAS诱发CVD的病理生理机制。1血压升高睡眠中呼吸暂停可导致机体缺氧，交感神经过度兴奋，血浆儿茶酚胺、肾素以及血管内皮素升高，导致血管痉挛；血管舒缩功能紊乱，可使血管平滑肌发生重构和肥厚，全身血管阻力增加；慢性缺氧时肾素—血管紧张素系统被激活，导致血压升高。1.2低氧血症OSAS患者气道阻力增加，造成气流中断、呼吸暂停，同时机体逐渐适应低氧环境，呼吸中枢对低氧和高碳酸血症敏感性下降，呼吸暂停次数增加，进一步加重机体缺氧。1.3脑自动调节功能下降正常人在体循环血压快速变化时，脑可通过自主调节功能产生保护效应，使脑血流量变化不大。

UMMARY:32 cases of hypertension were treated by acupuncturing the Fenglong(St.40, rich and prosperous) and Quchi(L.I.12, elbow crevice) acupoint. The content changes of these patients' plasma endotheliolysin and angiotensinⅡ were observated. The result showed that not only blood pressure but also plasma endotheliolysin could be lowered by acupuncture.

针刺曲池、丰隆穴治疗高血压病患者32例，并观察了患者自身治疗前后血浆内皮素和血管紧张素Ⅱ的含量，结果表明，针刺曲池、丰隆穴不仅能降低血压（P＜0.01），而且能降低其血桨内皮素水平（P＜0.05）；而治疗后患者血管紧张素Ⅱ较治疗前虽有所降低，但二者比较无统计学意义（P＞0.05）。

Although a single intracardial injection of an adenovirus containing the AT2R into male Sprague-Dawley rats did not affect the MAP, the effectiveness of an AT1R antagonist was greater in the AT2R-overexpressing animals compared with those expressing a control vector.7

虽然在雄性斯普拉-道来大鼠心内注射包含血管紧张素II受体血管紧张素II受体的腺病毒后没有观察到平均动脉压的上升，但是在血管紧张素II受体过度表达的个体血管紧张素I受体拮抗剂在血压调控中起到了更为有效的作用。

Thus, not only will it be important to assess the role of gonadal steroid regulation of AT2R action and the impact of AT2R mosaicism in BP control, we also need to determine whether the higher AT2R expression in the female is a result of escape from X inactivation.

因而我们不仅要评估性腺激素对于血管紧张素II受体影响以及血管紧张素II受体在血压调控中的作用，还要明确在女性中血管紧张素II受体的高表达是否与第二条X染色体的失活回避有关。

Because the renin-angiotensin system participate in not only humoral regulation of body fluid and systemic blood pressure but also structural and functional autoregulations in many tissues, we speculated that it may play a pivotal role in arterial structural and functional autoregulations, myocardial and renal adaptational changes due to simulated weightlessness.

我们推想局部肾素-血管紧张素系统(local renin-angiotensinsystem，L-RAS)在模拟失重引起的动脉、心肌和肾功能等的适应性变化中可能发挥关键性调节作用；且本室前一工作已发现4-wk模拟失重大鼠基底动脉与股动脉血管组织血管紧张素原(angiotensinogen，AGT)的基因表达分别呈增高与降低变化。

Under the direct current electric field, the expression of PDGFR were increased obviously and distributed asymmetricly on the membrane of VSMC. This receptor were mainly focused on the cathodal side of cellular membrane in electric field. The AT1R were also enhanced in the cells after exposure to the electric field, and the expression of AT2R had showed the changeless.

改进的电场干预装置作用下，血管平滑肌细胞膜血小板源生长因子受体表达增加，部分细胞内血小板源生长因子受体表达上调，呈不对称分布，在电场负极面较集中；细胞中血管紧张素Ⅱ1型受体表达亦增加，但无明显不对称分布现象；血管紧张素Ⅱ2型受体表达改变不显著。

As angiotensin II has a potent vasoconstrictive action, while bradykinin is a vasodilator, the reduced formation of angiotensin II and the inhibition of bradykinin breakdown leads to vasodilation.

由于血管紧张素Ⅱ有一个强有力的血管收缩的行动，而缓激肽是一种血管扩张，减少对血管紧张素 II 和形成的抑制缓激肽破裂导致血管扩张。

It has been postulated that Angiotensin Ⅱ type 2 receptor (AT2) functionally antagonizes ac 1 (AT1) receptor.

基于目前对血管紧张素Ⅱ2型受体（AT2）功能的认识，认为血管紧张素Ⅱ1型受体（AT1）和AT2受体有相互拮抗作用。

These drugs reduce blood pressure by blocking an enzyme that converts angiotensin to an active form that constricts blood vessels.

这些药物通过拦阻激活血管紧张肽的酶降低血压。血管紧张肽造成血管收缩。

They weren't aggressive, but I yelled and threw a rock in their direction to get them off the trail and away from me, just in case.

他们没有侵略性，但我大喊，并在他们的方向扔石头让他们过的线索，远离我，以防万一。

In slot 2 in your bag put wrapping paper, quantity does not matter in this case.

在你的书包里槽2把包装纸、数量无关紧要。