心血管活動(dòng)的體液調(diào)節(jié)

1、II . Humoral regulation of cardiovascular system 心血管活動(dòng)的體液調(diào)節(jié),,1. 腎素－血管緊張素－醛固酮系統(tǒng)(RAAS) 2. 腎上腺素和去甲腎上腺素 3. 血管升壓素 4. 血管內(nèi)皮生成的活性物質(zhì) 5. 心房鈉尿肽 6. 激肽釋放酶－激肽系統(tǒng),1. Renin-angiotension-aldosterone system(RAA腎素－血管緊

2、張素－醛固酮系統(tǒng)(RAAS),,交感神經(jīng)興奮低血壓Na＋↓,腎球旁細(xì)胞分泌腎素↑,血管緊張素原,AI,渴覺(jué),AII,ADH,心肌肥大血管增生,全身血管收縮,血容量↑,腎臟水鈉潴留,下丘腦,腎上腺皮質(zhì),醛固酮,,ACE,,,,,,,,,,,,,,,（1）Angiotonin II 血管緊張素II (AII),angiotensinogen ( α2-globulin) renin

3、 (kidney ) angiotensinⅠ(decapeptide)converting enzyme (pneumoangiogram) angiotensinⅡ(octapeptide) +AT1 receptorangiotensinase A angiotensin Ⅲ(heptapeptide),,,,a. The formation of an

4、giotonin 血管緊張素生成過(guò)程 血管緊張素原（肝合成） ↓腎素(腎近球細(xì)胞分泌） 血管緊張素Ⅰ（10肽） ↓(轉(zhuǎn)化酶,主要在肺血管) 血管緊張素Ⅱ（8肽）＋AT1受體 ↓血管緊張素酶A 血管緊張素III（7肽）,b. Physiological function of angiotensin Ⅱ

5、 血管緊張素Ⅱ的生理作用,① The systemic arterioles contracts and the peripheral resistance increases. 全身微動(dòng)脈收縮，外周阻力↑。② The veins contracts and the returned blood increases. 靜脈收縮，回心血量↑。,③ Prejunctional modulation,

6、promote the sympathetic nerve ending to excrete NA. 接頭前調(diào)制，促進(jìn)交感神經(jīng)末梢釋放NA。④ Action on the specific receptors of CNS , the sympathesis vasoconstrictor tone ↑. 作用于中樞特定受體，交感縮血管緊張↑。⑤ Stimulate the for

7、mation 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，水鈉重吸收↑，血壓↑。,(2) Aldosterone 醛固酮Synthesis position : adrenal cortex ZG cell合成部位：腎上腺皮質(zhì)

8、球狀帶細(xì)胞critical organ :distal tubule 、collecting duct靶器官：遠(yuǎn)曲小管、集合管Function: to keep Na+ and excrete K+ .作用：保Na+排K+作用。,,,mechanism of action作用機(jī)制,,醛固酮,促進(jìn)小管上皮細(xì)胞Na+ 泵運(yùn)轉(zhuǎn)促進(jìn)生化氧化提供ATP增加管腔膜對(duì)Na+ 通透性,,,,,,,,,,促進(jìn)Na+的主動(dòng)重吸收 (保Na

9、+),造成小管腔內(nèi)負(fù)電位,K+被分泌到小管液（排K+),,,,2. Adrenaline(Adr) and noradrenaline (NA) 腎上腺素和去甲腎上腺素 Synthesis postion: 合成部位（1）adrenal medulla 腎上腺髓質(zhì) Adr： 80%, NE ：20% 腎上腺素：80％，去甲腎上腺素 ：20％ （2）adrenergic n

10、erve ending 腎上腺素能神經(jīng)末梢 Secrete NA only. 僅分泌少量的NA入血。,腎上腺素 強(qiáng)心藥,去甲腎上腺素 升壓藥,3. vasopressin (Antidiuretic hormone ) 血管升壓素（抗利尿激素） Synthesis position： supraoptic nucleus and paraventricular nu

11、cleus. Store in posterior pituitary gland and release to blood stream. 合成部位：在下丘腦的視上核和室旁核合成。 在神經(jīng)垂體后葉貯存，釋放到血液中發(fā)揮作用。,,V1 receptor: constriction of blood vessel increase in blood

12、pressure. 結(jié)合V1受體：血管收縮,血壓↑。 V2 receptor: reabsorption of H2O from collecting duct increases. 結(jié)合V2受體：腎集合管對(duì)水的重吸收↑。,Physical function 生理功能 In normal condition , the incr

13、ease 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 f

14、luid .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.,正常情況下，血漿中ADH濃度升高時(shí)首先出現(xiàn)抗利尿效應(yīng)，當(dāng)其血漿濃度明顯升高時(shí)，才引起

15、血壓升高。ADH對(duì)體內(nèi)細(xì)胞外液量的調(diào)節(jié)起重要作用。在禁水、失水、失血等情況下，ADH釋放增加,保留體內(nèi)液體量，維持動(dòng)脈血壓。,4. Endothelium-derived vasoactive substances 血管內(nèi)皮生成的血管活性物質(zhì) (1) Endothelium-derived relaxing substances 血管內(nèi)皮生成的舒血管物質(zhì)Prostacyclin 前列環(huán)素（PGI

16、2)Endothelium-derived relaxing factor－ NO 血管內(nèi)皮舒張因子－一氧化氮（NO）,Endothelium-derived relaxing factor－ NO 血管內(nèi)皮舒張因子－一氧化氮（NO）,In 1977 Murad Find glycerol trinitrate educe its endothelium- relaxing effect through N

17、O. In 1980 Furchgott Presume Ach educe its its endothelium- relaxing effect through EDRF. In 1987 Moncada Certificate the EDRF is in fact NO through the way of “waterfall-type shower” .,The finding proc

18、ess of NO,NO的發(fā)現(xiàn)過(guò)程,1977年 默拉德（Murad） 確認(rèn)硝酸甘油類物質(zhì)舒張血管的作用通過(guò)釋放NO來(lái)實(shí)現(xiàn)。1980年 佛奇戈特(Furchgott) 推測(cè)Ach通過(guò)內(nèi)皮細(xì)胞釋放的EDRF來(lái)實(shí)現(xiàn)其舒血管效應(yīng)。1987年 蒙卡達(dá)(Moncada) 運(yùn)用“瀑布式淋浴”方法證明EDRF即是NO。,,Physical function of NONO的生理作用,,,,,AC,NOS,,,血管舒張,精氨酸,NO

19、,cGMP↑,[Ca2+]i↓,,瓜氨酸,↑NOS 活性：Ach，緩激肽，P物質(zhì)，5－HT,ATP↓NOS 活性：NA，ADH，AII,,Endothelin 內(nèi)皮素（ET) 21肽 Vascular endothelial cell excretes , strong vasoconstrictor. 血管內(nèi)皮細(xì)胞分泌的強(qiáng)縮血管物質(zhì)。 Endothelin causes first decrease in

20、BP and followed by long-term of the increase in BP. 內(nèi)皮素在引發(fā)長(zhǎng)時(shí)期血壓↑先出現(xiàn)血壓↓。,(2) Endothelium-derived vasoconstrictor substances 血管內(nèi)皮生成的縮血管物質(zhì),5. Atrial natriuretic peptide (ANP) 心房鈉尿肽(ANP),Synthesis po

21、sition:atrial muscle cell (28 peptides) 合成部位：心房肌細(xì)胞，28肽 Target organ: heart, blood vessels, kidney, CNS 靶器官：心臟，血管，腎臟，中樞 The blood volume increases, the atrium wall stretches →ANP↑ . 血容量增加，心房壁受到牽拉

22、→ANP↑ 。,Physiological function 生理作用,HR ↓,CO ↓ 心率↓，心輸出量↓。The blood vessel dilates and the peripheral resistance increases. 血管舒張，外周阻力↑。 To inhibit the activity of RAAS system,the secretion of water and sodium i

23、ncreases. 抑制RAAS系統(tǒng)的活性，腎排水排鈉↑。To inhibit the secretion of ADH . 抑制血管升壓素的釋放。,6. Kallikrein-kinin system 激肽釋放酶－激肽系統(tǒng)（KKS),組織激肽釋放酶,低分子激肽原,賴氨酰緩激肽,緩激肽,激肽酶I,激肽酶II,失活,高分子激肽原,血漿激肽釋放酶,氨基肽酶,,,,,,,,Callidin and kallidin is the

24、most intensive vessel- relaxing substances. Kinin can relax the VSM and improve the capillary permeability ,but as to other SM elicit contraction. 緩激肽和賴氨酰緩激肽（血管舒張素）是已知的最強(qiáng)烈的舒血管物質(zhì)。激肽可使血管平滑肌舒張和毛細(xì)血管通透性增高，但在其他

25、平滑肌則引起收縮。,III . Local regulation of blood flow 血流量的局部調(diào)節(jié) 1. Active hyperemia 主動(dòng)充血 2. Blood flow autoregulation 血流的自身調(diào)節(jié),The local regulation of blood flow is the organs and tissues to regul

26、ate its arteriole resistance and the blood flow depending on the factors of the organs and tissues but neural an hormonal mechanism. 血流量的局部調(diào)節(jié)是指器官或組織的微動(dòng)脈阻力或血流量的改變不取決于神經(jīng)和激素機(jī)制，而是取決于器官和組織本身的調(diào)節(jié)。,,1. Active hyperemia

27、 主動(dòng)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 acti

28、vity of organs and tissues strengthen. 大多數(shù)器官和組織代謝活動(dòng)增強(qiáng)時(shí)表現(xiàn)為血流量增加，稱為主動(dòng)充血。主動(dòng)充血是由于器官或組織活動(dòng)增強(qiáng)時(shí)微動(dòng)脈舒張的結(jié)果。,The relaxation of arteriole is the result of the change of the concentration of the chemical reconstituent in e

29、xtracellular fluid,which includes the decrease in OPP, the increase in the concentration of CO2, H+, adenosine, ATP etc. 主動(dòng)充血時(shí)導(dǎo)致微動(dòng)脈舒張的因素是微動(dòng)脈周圍的 細(xì)胞外液化學(xué)成份的改變。這些因素包括氧分壓降 低、 CO2濃度、H+濃度、腺苷、ATP等升高。,2. Blood flo

30、w autoregulation 血流量的自身調(diào)節(jié),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.

31、當(dāng)器官灌注壓發(fā)生變化時(shí)，該器官的微動(dòng)脈阻力也發(fā)生改變，使器官的血流量保持相對(duì)恒定的現(xiàn)象稱為血流量的自身調(diào)節(jié)。 器官：腎臟、心臟、腦,The mechanism of the blood flow autoregulation血流量自身調(diào)節(jié)的機(jī)制,代謝性機(jī)制 metabolism mechanism肌源性機(jī)制 muscle-derived mechanism,metabolism mechanism代謝性機(jī)制,BP

32、↓器官血流量↓,,氧分壓↓[CO2]，[ H+]↑,微動(dòng)脈舒張,血流量恢復(fù),,,,主動(dòng)充血：組織活動(dòng)增強(qiáng)→代謝產(chǎn)物增多→微血管舒張代謝性機(jī)制：血流量不足→代謝產(chǎn)物積聚 →微血管舒張,muscle-derived mechanism肌源性機(jī)制,血壓↑→牽張血管→平滑肌收縮→微動(dòng)脈阻力↑血壓↓→牽張血管→平滑肌舒張→微動(dòng)脈阻力↓,,,血容量恢復(fù),可能和平滑肌細(xì)胞膜上的牽拉敏感性鈣通道有關(guān)。,IV. Blood volume a

33、nd long term regulation of blood pressure 血量和動(dòng)脈血壓的長(zhǎng)期調(diào)節(jié) 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 t

34、he major factor influencing the long term regulation of BP . 神經(jīng)調(diào)節(jié)主要是在短時(shí)間內(nèi)血壓發(fā)生變化的情況下起 調(diào)節(jié)作用。動(dòng)脈血壓長(zhǎng)期調(diào)節(jié)的主要因素是血容量。,,Renal-body fluid control system 腎-體液控制系統(tǒng) (RAAS),The long term regulation of blood pressure is carr

35、ying out through the kidney to regulate the extracellular fluid volume, which is called Renal-body fluid control system .動(dòng)脈血壓的長(zhǎng)期調(diào)節(jié)是通過(guò)腎臟調(diào)節(jié)細(xì)胞外液量來(lái)實(shí)現(xiàn)的。這種機(jī)制又稱為腎－體液控制系統(tǒng)。 血容量↑→血壓↑→腎排水排Na+↑→血壓恢復(fù) 血容量↓→血壓↓→腎排水排Na+↓→

36、血壓恢復(fù),salt,Essential hypertension,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. 腎－體液控制系統(tǒng)調(diào)節(jié)血壓

37、的效能取決于血壓的變化對(duì)腎排水排鈉的影響。 From the normal level (100mmHg),the BP increased by 10mmHg, the excretion blood volume of kidney will increase by several times. 血壓從正常水平（100mmHg）每升高10mmHg，腎排泄量可增加數(shù)倍。,Influencing factor影響因素,1．

38、Vasopressin （ADH) 血管升壓素 (抗利尿激素） 循環(huán)血量↓ →ADH釋放↑ → 腎集合管重吸收↑ →細(xì)胞外液量↑ →BP↑ 2．RAAS系統(tǒng) 血管收縮，BP ↑AII 醛固酮→保鈉排鉀→水重吸收↑→細(xì)胞外液↑

39、 → BP ↑,,,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

40、 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.