心血管活动的体液调节.ppt

II . Humoral regulation of cardiovascular system 心血管活动的体液调节,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,1. Renin-angiotension-aldosterone system(RAA 肾素血管紧张素醛固酮系统(RAAS),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,AII,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,（1）Angiotonin II 血管紧张素II (AII),angiotensinogen ( 2-globulin) renin (kidney ) angiotensin(decapeptide) converting enzyme (pneumoangiogram) angiotensin(octapeptide) +AT1 receptor angiotensinase A angiotensin (heptapeptide),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（10肽） (转化酶,主要在肺血管) 血管紧张素（8肽）AT1受体 血管紧张素酶A 血管紧张素III（7肽）,b. Physiological function of angiotensin 血管紧张素的生理作用, The systemic arterioles contracts and the peripheral resistance increases. 全身微动脉收缩，外周阻力。 The veins contracts and the returned blood increases. 静脉收缩，回心血量。, 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。 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。 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。,(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。,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+),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。,肾上腺素 强心药,去甲肾上腺素 升压药,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。,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 H2O from collecting duct increases. 结合V2受体：肾集合管对水的重吸收。,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.,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。,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（PGI2) Endothelium-derived relaxing factor NO 血管内皮舒张因子一氧化氮（NO）,Endothelium-derived relaxing factor NO 血管内皮舒张因子一氧化氮（NO）,In 1977 Murad Find glycerol trinitrate educe its endothelium- relaxing effect through NO. 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 process of NO,NO的发现过程,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。 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。 1987年 蒙卡达(Moncada) 运用“瀑布式淋浴”方法证明EDRF即是NO。,Physical function of NO NO的生理作用,AC,NOS,血管舒张,精氨酸,NO,cGMP,Ca2+i,瓜氨酸,NOS 活性：Ach，缓激肽，P物质，5HT,ATP NOS 活性：NA，ADH，AII,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,5. Atrial natriuretic peptide (ANP) 心房钠尿肽(ANP),Synthesis position:atrial muscle cell (28 peptides) 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 ANP . 血容量增加，心房壁受到牵拉ANP 。,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。,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,氨基肽酶,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。,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,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。,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。,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 CO2, 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、 CO2浓度、H+浓度、腺苷、ATP等升高。,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,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,metabolism mechanism 代谢性机制,BP 器官血流量,氧分压 CO2， 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,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。,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。,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,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. 肾体液控制系统调节