Hypertension

Blood pressure（BP）: 血管内血流对血管壁产生的侧压力。 BP ＝CO×peripheral vascular resistence

Ⅰ concept of hypertension 是指血压调控障碍，使体 循环动脉血压持续升高的病理 过程。

完全清楚，以血压升高为主要表 现的一种独立的临床综合征。 1) essential hypertention classification of hypertension: 1) essential hypertention 占 95% 高血压的病因和发病机制尚不 完全清楚，以血压升高为主要表 现的一种独立的临床综合征。

2）secondary hypertension 因患其他疾病引起的血压升高， 血压升高只是疾病的一个主要症 状，称继发性高血压。

hypertension ≥ 140/90 mmHg judgement standard： Normal BP: ≤120/80 mmHg Prehypertension ≤ 139/89 mmHg hypertension ≥ 140/90 mmHg

Ⅱ Causes of essential hypertension 1.Genetic factors 1) 流行病学证据:

EH患者的年轻后代左室重量增加, 用 β1受体阻断剂(美多心安 50mg/d), 3月 后20% 的心脏改变复原，9月后90%的心 2)临床研究证据: EH患者的年轻后代左室重量增加, 用 β1受体阻断剂(美多心安 50mg/d), 3月 后20% 的心脏改变复原，9月后90%的心 脏改变被逆转。

2.环境与生活因素 同窝2日龄SHR正常饲养5周 高血压 暗室饲养5周 血压正常 自发高血压大鼠(SHR)， 暗室饲养5周 血压正常 自发高血压大鼠(SHR)， 以高蛋白、高钙、高钾、低钠饲养，血压 降低； 低蛋白、低钙、低钾、高钠饲养，血压显 著升高。

1979-1980年全国高血压普查： 北方患病率 > 6% (摄盐量: >15g/d) 南方(广西、福建) < 3% （摄盐量：<10g/d） 现有证据提示，EH即有多基因遗传、又 有单基因遗传的影响，并与多种环境因素密 切相关。 即：EH是遗传易感性和环境影响的产物。

Ⅲ pathogenesis of essential hypertension The main pathological change of essential hypertension: 1) convulsion and proliferation of smooth muscles in small arteries 2) artery remodeling

Narrow Lumen Onion Skin Thickening Of arterioles. why?

Ⅰ) abnormal of neurohumoral regulation 1. activation of sympathetic nervous system Evidence: ①patients of hypertension discharge of peripheral sympathetic nerves ②spontaneously hypertensive rats release increase of NE by sympathetic nerve, and increase of adrenalin in blood

Mechanism: ①intake of sodium excitation of sympathetic nervous system ② stress excitation of pallium excitation of sympathetic nervous center

③ heredity 2. activation of renin-angiotensin system(RAS) 高肾素型EH患者的比例 < 1/5 1)低肾素型EH存在RAS激活的证据 ①动物实验: 各种实验性高血压大鼠的动脉壁内肾素浓度 ②低肾素型EH患者用ACEI有效

③SHR用ACEI后血浆ACE达正常，BP降低滞后。BP降低与血管ACE活性的抑制相平行。 局部 RAS概念: 指存在于心脏、肾上腺、脑及血管壁中的RAS。 contraction of arteries action of NE, Endothelin-1 angiotensin accelerate expression of gene Ⅱ(ang Ⅱ) sympathetic center remodeling of arteries

3. contractive responsivity receptor of NE NE ET-1, AngⅡ, TXA2 NO, ANP, PGI2 4. low-responsivity of baroreceptor

Ⅱ) excretion of sodium by kidney 1. genetic defects of kidney ①glomeruler filtration rate(GFR) ②high-responsivity of renal arteries to vasoconstrictive substance ③reabsorption of sodium 2. results of defects of kidney Na+ and water in body

kinds of transmembrane Ⅲ) abnormal transmembrane transport of ions kinds of transmembrane transport of ions

1. abnormal transport of sodium Na+-K+ pump transport of Na+-K+ transport of Na+-Li+ intracellular [Na+] transport of Na+-H+ 2. abnormal transport of calium 　exchanges of Na+-Ca2+ intracellular calcium pump [Ca2+]

Membrane theory EH患者的细胞膜存在着特异性生化缺陷，因而膜的结构和功能异常，引起离子跨膜转运障碍，导致阳离子（特别是Ca2+）分布异常使血压升高。 血管平滑肌内[Ca2+]升高可能是高血压发病机制的最后共同途径。因此，高血压可能是一种细胞膜病。

Ⅳ) metabolic abnormity the main metabolic abnormity is insulin resistance the mechanism of low-responsivity of cells to insulin? insulin resistance blood sugar hyperinsulinism

Ⅴ) vascular remodeling? 　 utilizition of glucose results of Na+ pump reabsorption of Na+ insulin Ca2+ pump resistance release of catecholamine produce of NO from endothelium RAS Ⅴ) vascular remodeling?

Ⅳ causes and pathogenesis of secondary hypertension 1. renal hypertension cause ①vascular disease of kidney ②renal disease retention of water and sodium activation of RAS

2. Endocrine hypertension cause: disease of adrenal gland 3. Hypertension in pregnancy cause?

Ⅴ effect of hypertension 1. to induce atherosclerosis

Infarction of organs

Hemorrhage of organs

2. Hypertensive heart disease

3. Hypertensive nephropathy 4. Hypertensive Retinopathy

Normal Retina

Retinopathy