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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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Furthermore, recent studies have underlined that there are intricate interplays among adipocytes, the sympathetic nervous system, and the renin-angiotensin system, which participate in the obesity-associated dysmetabolic state.
最近的研究进一步揭示，在脂肪细胞、交感神经系统和肾素-血管紧张素系统之间存在密切的联系，其参与了肥胖相关的代谢失调状态。
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Hlubocka Z, Umnerova V, Hellers, et al. Is mild essential hypertension without obvious organ complications and rish factors associated with increased levels of circulating markers of endothelial dysfunction, effect of ACE inhibitor therapy.
当心衰发生和发展时，机体交感神经和肾素-血管紧张素系统激活，AngⅡ生成明显增多，AngⅡ与血浆内皮功能失调密切相关，能够刺激血管内皮细胞衍生ET-1释放，引起血管张力升高［6，7］。
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ejaculation：(射精)
4.射精(ejaculation)由性反应周期的持续期转入性高潮 期后,交感神经紧张性进一步增高,引起外尿道括约肌舒张,而尿道内括约肌仍保持紧张性收缩状态,以防止精液逆流入膀胱.
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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,