- 更多网络例句与血管紧张的相关的网络例句 [注：此内容来源于网络，仅供参考]
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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。
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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。
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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）。
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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。
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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。
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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。
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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。
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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。
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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。
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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。
- 更多网络解释与血管紧张的相关的网络解释 [注：此内容来源于网络，仅供参考]
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angiotensin：血管紧张肽
据调查.目前世界上的高血压患者数量可能已经超过10亿. 血管紧张肽原酶(renin)-血管紧张肽(angiotensin)系靶向候选新药的开发正在不断推进. [第一段]
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angiotensin：血管紧张素
据心脏专科医生解释,腹腔内脂肪与皮下脂肪是不同的,它本身可以产生一些化学物,使以下荷尔蒙发生变化:(1)血管紧张素(Angiotensin)分泌增多:引致血管收缩,令血压增高;(2)轻素(也称瘦素,Leptin)失灵:"轻素"负责指挥脑神经控制胃,
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heparin：肝素 肝素
二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)肝素 肝素(heparin) 是带大量负电荷的大分子,不易通过生物膜,口服不被吸收,常静脉给药. 通常将前列腺素、组胺、5-羟色胺、白三烯和血管活性肽类(P物质、激肽类、血管紧张素、利尿钠肽、血管活性肠肽、降钙素基因相关肽、神经肽Y和内皮素等)以及NO和腺苷等称之为自体活性物质(autocoi
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limpet：帽贝
主要源自于一个专一性针对名为血管紧张素(angiotensin)的蛋白质作用的分子的发现,就过去相关的研究数据显示angiotensin是肝脏所产生,它会透过窄化动脉的方式升高血管里的压力,而这个高血压疫苗的研究计划,成功的从帽贝 (limpet)的体内,纯化出一种特定的蛋白质,
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cardiac remodeling：心肌重塑
④中性内肽酶(NEP)/血管紧张素(ACE)双重抑制剂:慢性心力衰竭(CHF)发生发展的病理基础是心肌重塑(cardiac remodeling),在初始的心肌损伤后,有多种的内源性神经、内分泌和细胞因子的激活,包括交感神经系统(SNS)及肾素-血管紧张素-醛固酮系统(RAAS)过度激活和白介素1、6,
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anaerobiotic：厌氧的,厌气的,厌气生活的
achiote胭脂树工;胭脂树种子 | anaerobiotic厌氧的,厌气的,厌气生活的 | angiotensin血管紧张素,血管紧张肽
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angiotonic：血管紧张的
angiotelectasis 毛细血管扩张 | angiotonic 血管紧张的 | angiotribe 血管压轧钳
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angiotribe：血管压轧钳
angiotonic 血管紧张的 | angiotribe 血管压轧钳 | angiotripsy 血管压轧术
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vasotonic：[生理]血管紧张的
acceptable currency 可接受的货币 | vasotonic [生理]血管紧张的 | double issue 合刊
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ARB：血管紧张素受体阻滞剂
而检查结果为阴性的患者新华社信息北京12月15日电 美国阿拉巴马大学的研究人员认为,在已 经应用包括一种利尿剂和一种血管紧张素转换酶(ACE)抑制剂或血管紧张素受 体阻滞剂(ARB)在内的多药物方案的伴或不伴原发性醛固酮增多症患者中,