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II. Humoral regulation of cardiovascular system 心血管活动的体液调节.

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Presentation on theme: "II. Humoral regulation of cardiovascular system 心血管活动的体液调节."— Presentation transcript:

1 II. Humoral regulation of cardiovascular system 心血管活动的体液调节

2 1. 肾素-血管紧张素-醛固酮系统 (RAAS) 2. 肾上腺素和去甲肾上腺素 3. 血管升压素 4. 血管内皮生成的活性物质 5. 心房钠尿肽 6. 激肽释放酶-激肽系统

3 1. Renin-angiotension-aldosterone system(RAA 肾素-血管紧张素-醛固酮系统 (RAAS)

4 交感神经兴奋 低血压 Na + ↓ 肾球旁细胞 分泌肾素 ↑ 血管紧 张素原 AI 渴觉 A II ADH 心肌肥大 血管增生 全身血 管收缩 血容量 ↑ 肾脏水 钠潴留 下丘脑 肾上腺皮质 醛固酮 ACE

5 ( 1 ) Angiotonin II 血管紧张素 II (AII) angiotensinogen ( α2-globulin) renin (kidney ) angiotensin Ⅰ (decapeptide) converting enzyme (pneumoangiogram) angiotensin Ⅱ (octapeptide) +AT 1 receptor angiotensinase A angiotensin Ⅲ (heptapeptide)

6 a. The formation of angiotonin 血管紧张素生成过程 血管紧张素原 (肝合成) ↓ 肾素 ( 肾近球细胞分泌) 血管紧张素Ⅰ ( 10 肽) ↓ ( 转化酶, 主要在肺血管 ) 血管紧张素Ⅱ ( 8 肽)+ AT 1 受体 ↓ 血管紧张素酶 A 血管紧张素 III ( 7 肽)

7 b. Physiological function of angiotensin Ⅱ 血管紧张素Ⅱ的生理作用 ① The systemic arterioles contracts and the peripheral resistance increases. 全身微动脉收缩,外周阻力 ↑ 。 ② The veins contracts and the returned blood increases. 静脉收缩,回心血量 ↑ 。

8 ③ Prejunctional modulation, promote the sympathetic nerve ending to excrete NA. 接头前调制,促进交感神经末梢释放 NA 。 ④ Action on the specific receptors of CNS, the sympathesis vasoconstrictor tone ↑. 作用于中枢特定受体,交感缩血管紧张 ↑ 。 ⑤ Stimulate the formation and excretion of aldosterone , the reabsorption of sodium and fluid increases and thus the BP increases too. 刺激醛固酮生成分泌,水钠重吸收 ↑ ,血压 ↑ 。

9 (2) Aldosterone 醛固酮 Synthesis position : adrenal cortex ZG cell 合成部位:肾上腺皮质球状带细胞 critical organ :distal tubule 、 collecting duct 靶器官:远曲小管、集合管 Function: to keep Na + and excrete K +. 作用:保 Na + 排 K + 作用。

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11 mechanism of action 作用机制 醛固酮 促进小管上皮细胞 Na + 泵运转 促进生化氧化提供 ATP 增加管腔膜对 Na + 通透性 促进 Na + 的主动 重吸收 ( 保 Na + ) 造成小管腔 内负电位 K + 被分泌到 小管液(排 K + )

12 2. Adrenaline(Adr) and noradrenaline (NA) 肾上腺素和去甲肾上腺素 Synthesis postion: 合成部位 ( 1 ) adrenal medulla 肾上腺髓质 Adr : 80%, NE : 20% 肾上腺素: 80 %,去甲肾上腺素 : 20 % ( 2 ) adrenergic nerve ending 肾上腺素能神经末梢 Secrete NA only. 仅分泌少量的 NA 入血。

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14 肾上腺素 强心药

15 去甲肾上腺素 升压药

16 3. vasopressin (Antidiuretic hormone ) 血管升压素(抗利尿激素) Synthesis position : supraoptic nucleus and paraventricular nucleus. Store in posterior pituitary gland and release to blood stream. 合成部位:在下丘脑的视上核和室旁核合成。 在神经垂体后叶贮存,释放到血液中发挥作用。

17 V1 receptor: constriction of blood vessel increase in blood pressure. 结合 V1 受体:血管收缩, 血压 ↑ 。 V2 receptor: reabsorption of H 2 O from collecting duct increases. 结合 V2 受体:肾集合管对水的重吸收 ↑ 。

18 Physical function 生理功能 In normal condition, the increase in the level of ADH in plasma firstly induces the effect of antidiuresis,and only when its level increases definitely,the BP increases. ADH plays an important role in the regulation of the volume of extracellular fluid.Under the condition of water bearing, water depletion and blood loss,the secretion of ADH increases to keep the normal volume of body fluid and maintain the normal BP.

19 正常情况下,血浆中 ADH 浓度升高时首先出现抗 利尿效应,当其血浆浓度明显升高时,才引起血 压升高。 ADH 对体内细胞外液量的调节起重要作 用。在禁水、失水、失血等情况下, ADH 释放增 加, 保留体内液体量,维持动脉血压。

20 4. Endothelium-derived vasoactive substances 血管内皮生成的血管活性物质 (1) Endothelium-derived relaxing substances 血管内皮生成的舒血管物质 Prostacyclin 前列环素( PGI 2 ) Endothelium-derived relaxing factor - NO 血管内皮舒张因子-一氧化氮( NO )

21 Endothelium-derived relaxing factor - NO 血管内皮舒张因子-一氧化氮( NO )

22 In 1977 Murad In 1977 Murad Find glycerol trinitrate educe its endothelium- Find glycerol trinitrate educe its endothelium- relaxing effect through NO. relaxing effect through NO. In 1980 Furchgott In 1980 Furchgott Presume Ach educe its its endothelium- relaxing effect through EDRF. Presume Ach educe its its endothelium- relaxing effect through EDRF. In 1987 Moncada In 1987 Moncada Certificate the EDRF is in fact NO through the Certificate the EDRF is in fact NO through the way of “waterfall-type shower”. way of “waterfall-type shower”. The finding process of NO

23 NO 的发现过程 1977 年 默拉德( Murad ) 1977 年 默拉德( Murad ) 确认硝酸甘油类物质舒张血管的作用通过释放 NO 来 实现。 确认硝酸甘油类物质舒张血管的作用通过释放 NO 来 实现。 1980 年 佛奇戈特 (Furchgott) 1980 年 佛奇戈特 (Furchgott) 推测 Ach 通过内皮细胞释放的 EDRF 来实现其舒血管 效应。 推测 Ach 通过内皮细胞释放的 EDRF 来实现其舒血管 效应。 1987 年 蒙卡达 (Moncada) 1987 年 蒙卡达 (Moncada) 运用 “ 瀑布式淋浴 ” 方法证明 EDRF 即是 NO 。 运用 “ 瀑布式淋浴 ” 方法证明 EDRF 即是 NO 。

24 Physical function of NO NO 的生理作用

25 AC NOS 血管舒张精氨酸 NOcGMP↑[Ca2+]i↓ 瓜氨酸 ↑NOS 活性: Ach ,缓激肽, P 物质, 5 - HT,ATP ↓NOS 活性: NA , ADH , AII

26 Endothelin 内皮素( ET) 21 肽 Vascular endothelial cell excretes, strong vasoconstrictor. 血管内皮细胞分泌的强缩血管物质。 Endothelin causes first decrease in BP and followed by long-term of the increase in BP. 内皮素在引发长时期血压 ↑ 先出现血压 ↓ 。 (2) Endothelium-derived vasoconstrictor substances 血管内皮生成的缩血管物质

27 5. Atrial natriuretic peptide (ANP) 5. Atrial natriuretic peptide (ANP) 心房钠尿肽 (ANP) Synthesis position:atrial muscle cell (28 peptides) Synthesis position:atrial muscle cell (28 peptides) Target organ: heart, blood vessels, kidney, CNS 合成部位:心房肌细胞, 28 肽 Target organ: heart, blood vessels, kidney, CNS 靶器官:心脏,血管,肾脏,中枢 The blood volume increases, the atrium wall stretches The blood volume increases, the atrium wall stretches →ANP↑. →ANP↑. 血容量增加,心房壁受到牵拉 →ANP↑ 。

28 Physiological function 生理作用 HR ↓,CO ↓ 心率 ↓ ,心输出量 ↓ 。 The blood vessel dilates and the peripheral resistance increases. 血管舒张,外周阻力 ↑ 。 To inhibit the activity of RAAS system,the secretion of water and sodium increases. 抑制 RAAS 系统的活性,肾排水排钠 ↑ 。 To inhibit the secretion of ADH. 抑制血管升压素的释放。

29 6. Kallikrein-kinin system 激肽释放酶-激肽系统( KKS) 组织激肽释放酶 低分子激肽原赖氨酰缓激肽 缓激肽 激肽酶 I 激肽酶 II 失活 高分子激肽原 血浆激肽释放酶

30 Callidin and kallidin is the most intensive vessel- relaxing substances. Kinin can relax the VSM and improve the capillary permeability,but as to other SM elicit contraction. 缓激肽和赖氨酰缓激肽(血管舒张素)是已知的最强烈 的舒血管物质。激肽可使血管平滑肌舒张和毛细血管 通透性增高,但在其他平滑肌则引起收缩。

31 III. Local regulation of blood flow 血流量的局部调节 1. Active hyperemia 主动充血 2. Blood flow autoregulation 血流的自身调节

32 The local regulation of blood flow is the organs and tissues to regulate its arteriole resistance and the blood flow depending on the factors of the organs and tissues but neural an hormonal mechanism. 血流量的局部调节是指器官或组织的微动脉阻力或血 流量的改变不取决于神经和激素机制,而是取决于器 官和组织本身的调节。

33 1. Active hyperemia 主动充血 The phenomenon of the increase in the blood flow in most organs and tissues when their metabolism activity strengthen is called active hyperemia.It is caused by the relaxation of arterioles as a result of the activity of organs and tissues strengthen. 大多数器官和组织代谢活动增强时表现为血流量增加, 称为主动充血。主动充血是由于器官或组织活动增强 时微动脉舒张的结果。

34 The relaxation of arteriole is the result of the change of the concentration of the chemical reconstituent in extracellular fluid,which includes the decrease in OPP, the increase in the concentration of CO 2, H +, adenosine, ATP etc. 主动充血时导致微动脉舒张的因素是微动脉周围的 细胞外液化学成份的改变。这些因素包括氧分压降 低、 CO 2 浓度、 H + 浓度、腺苷、 ATP 等升高。

35 2. Blood flow autoregulation 血流量的自身调节 When the organ perfusion pressure changes, the arteriole resistance also change to keep the organ blood flow at a constant level, which is called the autoregulation of the blood flow. 当器官灌注压发生变化时,该器官的微动脉阻力也 发生改变,使器官的血流量保持相对恒定的现象称 为血流量的自身调节。 器官:肾脏、心脏、脑

36 The mechanism of the blood flow autoregulation 血流量自身调节的机制 代谢性机制 metabolism mechanism 肌源性机制 muscle-derived mechanism

37 metabolism mechanism 代谢性机制 ↓ BP ↓ ↓ 器官血流量 ↓ ↓ 氧分压 ↓ [] , []↑ [ CO 2 ] , [ H + ]↑ 微动脉舒张血流量恢复 主动充血:组织活动增强 → 代谢产物增多 → 微血管舒张 代谢性机制:血流量不足 → 代谢产物积聚 → 微血管舒张

38 muscle-derived mechanism 肌源性机制 血压 ↑→ 牵张血管 → 平滑肌收缩 → 微动脉阻力 ↑ 血压 ↓→ 牵张血管 → 平滑肌舒张 → 微动脉阻力 ↓ 血容量 恢复 可能和平滑肌细胞膜上的牵拉敏感性钙通道有关。

39 IV. Blood volume and long term regulation of blood pressure 血量和动脉血压的长期调节 Neural regulation mainly plays a role in the regulation of BP under the condition of the transient fluctuation of BP,and the blood volume is the major factor influencing the long term regulation of BP. 神经调节主要是在短时间内血压发生变化的情况下起 调节作用。动脉血压长期调节的主要因素是血容量。

40 Renal-body fluid control system 肾 - 体液控制系统 (RAAS) The long term regulation of blood pressure is carrying out through the kidney to regulate the extracellular fluid volume, which is called Renal-body fluid control system. 动脉血压的长期调节是通过肾脏调节细胞外液量来 实现的。这种机制又称为肾-体液控制系统。 ↑↑↑ 血容量 ↑→ 血压 ↑→ 肾排水排 Na + ↑→ 血压恢复 血容量 ↓→ 血压 ↓→ 肾排水排 Na + ↓→ 血压恢复

41 salt Essential hypertension

42 The efficacy of renal-body fluid control system to regulate the BP is determined by the influence of the fluctuation of BP to the excretion of sodium and water of kidney. 肾-体液控制系统调节血压的效能取决于血压的变化 对肾排水排钠的影响。 From the normal level (100mmHg),the BP increased by 10mmHg, the excretion blood volume of kidney will increase by several times. 血压从正常水平( 100mmHg )每升高 10mmHg ,肾 排泄量可增加数倍。

43 影响因素 Influencing factor 影响因素 1 . Vasopressin ( ADH) 血管升压素 ( 抗利尿激素) 血管升压素 ( 抗利尿激素) 循环血量 ↓ →ADH 释放 ↑ → 肾集合管重吸收 ↑ 循环血量 ↓ →ADH 释放 ↑ → 肾集合管重吸收 ↑ → 细胞外液量 ↑ →BP↑ → 细胞外液量 ↑ →BP↑ 2 . RAAS 系统 血管收缩, BP ↑ AII 醛固酮 → 保钠排钾 → 水重吸收 ↑ → 细胞外液 ↑ 醛固酮 → 保钠排钾 → 水重吸收 ↑ → 细胞外液 ↑ → BP ↑ → BP ↑

44 In summarize , the regulation of BP is an intricate process which relates to many mechanisms.The neural regulation is quick and short-term which is carried out through the regulation of the diameter of resistance vessels and cardiac activation.However the long term regulation of BP is mainly undertaken through the regulation of kidney to the circulation blood volume. In summarize , the regulation of BP is an intricate process which relates to many mechanisms.The neural regulation is quick and short-term which is carried out through the regulation of the diameter of resistance vessels and cardiac activation.However the long term regulation of BP is mainly undertaken through the regulation of kidney to the circulation blood volume. 总之,血压的调节是一个复杂的、多种机制参与的 过程。神经调节一般是快速的、短期内的调节,主 要是通过对阻力血管口径及心脏活动的调节来实现 的,而长期调节则主要是通过肾对循环血量的调节 实现的。 总之,血压的调节是一个复杂的、多种机制参与的 过程。神经调节一般是快速的、短期内的调节,主 要是通过对阻力血管口径及心脏活动的调节来实现 的,而长期调节则主要是通过肾对循环血量的调节 实现的。

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