Microsoft PowerPoint - 08-kidney3-yu-2017-ENG [兼容模式]

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1 Kidney Physiology II YU Yanqin ( 虞燕琴 ), Zhejiang University, School of Medicine

2 Urinary concentration and dilution Concentrative urine 浓缩尿 : Osmolality of urine > plasma osmolality (300mOsm/L H 2 O) Diluted urine 稀释尿 : Osmolality of urine < plasma osmolality

3 Formation of Diluted Urine Isosmotic reabsorption of water at proximal tubule Impermeable of water at thick ascending limb ADH Reabsorption of water at distal tubule and collecting duct Diluted urine

4 Formation of Concentrative Urine ADH Reabsorption of water at distal tubule and collecting duct Concentrative ti Urine ADH---key element of urinary concentration and dilution What is the drive force of water reabsorption at distal tubule and collecting duct?

5 The Osmotic Gradient of the Renal Medulla

6 Formation of Osmotic Gradient of the Renal Medulla Permeability of the Tubular System

7 Permeability bl of the Tubular System H 2 O NaCl Thin descending ++ limb Thick ascending limb Thin ascending limb Distal tubule _ Actively transport _ ADH Actively transport Urea Cortical collecting duct Inner medullary collecting duct + ADH Actively transport + ADH Actively transport ++ _

8 Formation of Osmotic Gradient of the Renal Medulla The countercurrent theory H 2 O 1. Countercurrent Na + multiplication 逆流倍增 A B C

9 肾髓质浓度梯度形成机制可用逆流交换与逆流倍增系统模型来解释 : 1. 髓袢和集合管形态与功能类似于物理学中的逆流倍增模型 2. 直小血管的结构形状和功能类似于逆流交换模型

10 1.Countercurrent multiplication H 2 O Na +

11 Establishing of Osmotic Gradient of the Renal Medulla Outer medulla: reabsorption of NaCl at thick ascending limb hyperosmolality Inner medulla: 1) urea recycling 2) reabsorption of NaCl at thin ascending limb hyperosmolality

12 Urea recycling Urinary concentration and dilution.swf

13 The Countercurrent t Theory 2. Countercurrent exchange 逆流交换

14 2. Countercurrent exchange

15 Vasa recta Maintenance of the Osmotic Gradient in the Medulla

16 Maintenance of the Osmotic Gradient in the Medulla The vasa recta: Countercurrent exchanger

17 Summary: Formation of Concentrated or Dilute Urine In the presence of ADH Collecting duct permeable to water excretion of a concentrated urine In the absence of ADH Collecting duct impermeable to water excretion of a diluted urine

18 Factors that affect the concentration and dilution of the urine 1) Damage of renal medulla Resulting in an impairment of the concentrating ability 2) Loop diuretics such as frusemide, inhibiting the Na + /K + /2Cl - co- transport system in the thick ascending limb

19 Factors that affect the concentration and dilution of the urine 3) Lack of urea in the body such as malnutrition, reducing the osmotic gradient established in the renal medulla 4) Increased velocity of blood flow in the vasa recta carrying away amount of NaCl reducing the osmotic gradient in the medulla

20 Humoral Control of Renal Functions Antidiuretic hormone ( 抗利尿激素,ADH) Synthesis in supraoptic and paraventricular nuclei ( 视上核与室旁核 ) Release from the posterior pituitary

21 Mechanism of ADH Antidiuresis Increasing water permeability of collecting duct Insertion of aquaporins 水通道 in apical membrane

22 Diabetes Insipidous 尿崩症

23 Regulation of ADH Release e Plasma osmolality Plasma osmolality (+)hypothalamic osmoreceptors production and release of ADH urine Blood volume Blood volume (+)baroreceptor reflex & atrial stretch receptors ADH release urine Blood volume

24 Water diuresis i 水利尿 Physiologic water diuresis is a response to water load: Slightly decreased plasma osmolality (drinking bulk water) ADH Increased urine flow until plasma osmolality increases

25 Humoral Control of Renal Functions Aldosterone 醛固酮 Secreted by the glomerulosa 球状带 of the adrenal cortex To increase the reabsorption of Na + in the distal tubule and early collecting duct, coupled to secretion of K +

26 Mechanism of Aldosterone Action To increase number of Na + channels To increase activity of Na + pumps

27 Regulation of Aldosterone Secretion 1. Renin- Angiotensin System ( 肾素 - 血管紧张素系统 )

28 Regulation of Aldosterone Secretion 2. Plasma concentrations of sodium and potassium [K + ] Aldosterone secretion [Na + ] Aldosterone secretion 3. Adrenocorticotrophin t ( 促肾上腺皮质激素,ACTH) Necessary for Aldosterone secretion, but little effect in controlling the secretion rate

29 Ingesting too much potassium stimulates aldosterone secretion from the adrenal cortex; aldosterone increases sodium reabsorption at the expense of increased potassium secretion. Also shown here is an indication that more potassium in the filtrate leads to greater potassium excretion in the urine.

30 Decreased blood volume and ingesting too much potassium both stimulate aldosterone secretion from the adrenal cortex; aldosterone increases sodium reabsorption at the expense of increased potassium secretion.

31 Humoral Control of Renal Functions Atrial natriuretic peptides ( 心房钠尿肽, ANP) Synthesis in the cardiac atrial muscle cell Leading to increased excretion of salt & water Its mechanism:

32 Regulation of ANP Release Stretch of the atrium Extracellular fluid volume and blood volume Plasma sodium concentration

33 Renal Clearance 血浆清除率 Defined as the volume of plasma required to supply the amount of a substance X to be excreted in urine per unit time Cx Ux * V Px

34 Micturition 排尿 Innervation of the bladder and urethra

35 Micturition

36 Micturition Innervation of the bladder and urethra 1) Parasympathetic pelvic nerves 盆神经 To cause contraction of the detrusor muscle of the bladder and opening of the internal sphincter 2) Sympathetic hypogastric nerves 腹下神经 To induce closure of the internal sphincter 3) Somatic pudendal nerves 阴部神经 To induce contraction of the external sphincter

37 Micturition i i Reflex Micturition occurs when the intravesicular pressure reaches 70 cmh 2 O via a reflex action P det, cm H 2 O volume 300 ml

38 Higher Control of Micturition Inhibitory and facilitatory centers in the cerebral cortex and pons

39 Pathways of Micturition iti Reflex

40 Micturition i i reflex 膀胱内尿量达 400~500ml 膀胱壁的牵张感受器 (+) 盆神经骶髓的排尿反射初级中枢脑干和大脑皮层的排尿反射高级中枢尿意盆神经逼尿肌收缩, 内括约肌松弛排尿入尿道外括约肌松弛排尿反射 ( 正反馈 ) 尿液排完

41 Micturition iti reflex

42 Enuresis 遗尿尿储留尿失禁

43 Summary Terms: Water diuresis Renal clearance List the factors that affect the concentration and dilution of the urine

44 General Question What are the change of urine and its mechanism when one sweats a great deal and drinks little water?

45 Intensive Reading Textbook of Medical Physiology (Guyton & Hall) Page 309 Page Page

46 Questions 1. 血浆渗透压的变化对肾脏泌尿的生理功能有何影响? 2. 大量出汗而饮水过少时, 尿液有何变化? 其机制如何? 3.3Kg 体重的家兔, 耳缘静脉注射 20% 葡萄糖溶液 5ml,, 尿液有何变化? 简述其变化机制 4. 通常情况和紧急情况下, 肾血流量是如何调节的? 各有何重要生理意义? 5. 试述肾脏的泌尿功能在维持机体内环境稳定中的作用 6. 简述直小血管的血流速度对尿液生成的影响 7. 为什么说髓袢升支粗段主动吸收 NaCl 是形成髓质高渗的动力? 8. 体循环血压明显降低时对尿液生成有何影响? 9. 影响肾小球滤过作用的因素有哪些?

47 血浆渗透压的变化对肾脏泌尿的生理功能有何影响? 1.. 血浆胶体渗透和晶体渗透压变化时均可影响肾脏的尿生成, 但各自的机理不同 ⑴ 血浆胶体渗透压一般维持稳定, 如因某种原因使之降低, 肾小球有效滤过压将升高, 原尿生成增多, 尿排出量增加 ; 血浆胶体渗透压升高时, 与上述作用相反, 可使尿量减少 ⑵ 血浆晶体渗透升高时, 可刺激位于下丘脑前部室周器的渗透压感受器, 引起 ADH 的合成和释放增加, 远曲小管和集合管对水的通透性增加, 水重吸增加, 排出尿量减少 ; 而晶体渗透压降低时, 作用相反, 使排出的尿量增加, 如水利尿产生的原理即为血浆晶体渗透压降低所致

48 大量出汗而饮水过少时, 尿液有何变化? 其机制如何? 2.. 汗为低渗溶液, 大量出汗而饮水过少时, 尿液排出量减少, 其渗透压升高大量出汗 :(1) 组织液晶体渗透压升高, 水的渗透作用使血浆晶体渗透压也升高, 下丘脑渗透压感受器兴奋 (2) 血容量减少, 心房及胸内大静脉血管的容积感受器对视上核和旁室核的抑制作用减弱上述两种途径均使视上核和旁室核合成和分泌 ADH 增加, 血液中 ADH 浓度升高, 使远曲小管和集合管对水的通透性增加, 水重吸收增加, 尿量减少, 尿渗透压升高此外, 大量出汗, 还可能使血浆胶体渗透压升高, 肾小球有效滤过压降低, 原尿生成减少, 尿量减少

49 3Kg 体重的家兔, 耳缘静脉注射 20% 葡萄糖溶液 5ml,, 尿液有何变化? 简述其变化机制 3.. 尿量增加, 尿液渗透压变化不明显 3Kg 家兔, 血液量约 240ml,, 注入血中的葡萄糖为 5ml 20%=1( ( 克 ), 将使血糖升至约 500mg/100ml,, 明显超过肾糖阈, 导致远曲小管和集合管小管液内含大量的葡萄糖, 阻碍水的重吸收, 产生渗透性利尿, 尿量增加, 出现糖尿, 但尿液渗透压变化不明显

50 通常情况和紧急情况下, 肾血流量是如何调节的? 各有何重要生理意义? 4.. 安静情况下, 血压基本稳定, 肾动脉压波动在 mmHg(10 180mmHg( Kpa) 范围内, 通过肾脏的自身调节, 维持肾血流量稳定, 从而保证了肾脏的泌尿功能当机体受到强烈刺激时, 如大出血, 将使交感 - 肾上腺髓质系统强烈兴奋, 产生应急反应, 使肾血管特别是入球动脉收缩, 肾血流量减少, 有效滤过压也降低, 滤过减少而重吸收增加, 尿量减少, 既能维持一定的血容量, 又能使血液重新分配, 对于紧急情况下保证心脑重要器官的血液供应具有重要意义

51 试述肾脏的泌尿功能在维持机体内环境稳定中的作用 5.. 肾脏的泌尿功能表现在对代谢终产物及其他无用物质的排泄, 而吸收和保留机体需要的物质, 参与机体水盐平衡, 酸碱平衡的调节, 有效地维持机体内环境的稳定 ⑴ 在中枢神经的参与下, 根据机体对水的需求, 通过 ADH,, 调节远曲小管和集合管对水的通透性, 维持水代谢的平衡和血容量的稳定 ⑵ 体内许多电解质浓度的维持, 受肾脏的调节, 如 Na+ K+ Ca2+ 等, 当 Na+/ K+ 降低时, 醛固醇分泌增加, 肾脏保 Na+ 排 K+ 作用增强, 使 Na+/ K+ 恢复正常 ; 当 Na+/ K+ 升高时, 情况相反, 从而使 Na+ K+ 维持在较恒定的水平此外对 Ca2+ 也有调节作用 ⑶ 酸中毒时, 体内 H+ 增加 :1 肾内碳酸酐酶活性增强, 肾 HCO3- 重吸收增加 2H+ H+- Na+ 交换增强, 肾排 H+ 增加 3 NH3 分泌增加,NH4Cl 排出增加使体内 [H+] 降低, 恢复酸碱平衡碱中毒时情况相反, 从而使体内 ph 维持在相对稳定的水平

52 6. 简述直小血管的血流速度对尿液生成的影响 6.. 肾远曲小管和集合管不断重吸收水和其它物质, 将破坏肾髓质高渗状态, 影响泌尿功能肾髓质直小血管的血供特点, 能及时将重吸收的物质和水分带回血液, 维持肾髓质的高渗状态如果直小血管血流减慢, 重吸收的水分不能及时运至血液循环, 使髓质渗透压下降而当其中的血流增快时, 将过多地带走髓质内的 NaCl 和尿素, 也会使髓质渗透压降低故直小血管中血流过慢和过快, 都将影响尿液的生成所以, 稳定的直小血管血流, 是维持肾髓质高渗的必要条件和影响尿液生成的重要因素

53 为什么说髓袢升支粗段主动吸收 NaCl 是形成髓质高渗的动力? 7.. 引起肾髓质高渗的 NaCl 和尿素来自小管液肾小管和集合管各段对管各段对 H2O NaCl 和尿素的通透性和转运方式不同降支细段对 H2O 通透, 对 NaCl 和尿素不通透 ; 升支细段对 NaCl 和尿素通透, 对水不通透, 升支粗段主动吸收 NaCl 而对水和尿素不通透 ; 内髓集合管允许尿素通透小管液流经升支粗段, 主动吸收 NaCl,, 产生外髓高渗, 浓缩管内尿素 ; 内髓集合管中高浓度的尿素向管外扩散, 形成内髓高渗 ; 降支细段 H2O 进入髓质,NaCl 被浓缩 ; 升支细段 NaCl 向外扩散, 内髓渗透压进一步升高, 形成髓质高渗若抑制升支粗段主动吸收 NaCl,, 外髓高渗不能形成, 尿素和 NaCl 不被浓缩, 内髓渗透压也不能升高故升支粗段主动重吸收 NaCl 是形成髓质高渗的动力

54 体循环血压明显降低时对尿液生成有何影响? 8.. 体循环血压因某种原因明显降低, 使肾动脉血压低于 80mmHg(10.7Kpa) 时, 尿排出量将减少 (1) 体循环血压下降, 减压反射减弱, 交感神经兴奋, 引起应急反应, 入球动脉收缩, 滤过减少 (2) 血压下降, 血容量相对不足, 视上核和室旁核合成和释放 ADH 增加, 肾远曲小管和集合管对水的重吸收增多, (3) 血压下降, 肾素 - 血管紧张素 - 醛固酮系统活动增强, 醛固酮分泌增加, 促进肾保 Na+ 排 K+ 和对水的重吸收以上三方面的共同作用, 使尿量减少

55 影响肾小球滤过作用的因素有哪些? 9.. 肾小球滤过作用主要受下列因素的影响 : (1) 滤过膜的通透性即膜孔的大小和滤过膜上负电荷的多少 (2) 滤过面积的大小在其它因素不变的情况下, 面积越小, 单位时间滤过量也越少 (3) 肾小球有效滤过压包括肾小球毛细血管内压的高低, 血浆胶体渗透压和肾小囊内压, 它们的代数和的大小是影响滤过的主要因素 (4) 肾小球血浆流量其它因素不变时, 肾小球血浆流量增加, 滤过量也增加, 血浆流量减少, 滤过量也减少

日文技術用語

日文技術用語泌尿系統 16-1 1. 菊糖 (inulin) 常被用以測量哪一種生理參數? (A) 腎絲球過濾率 (B) 腎血漿流量 (C) 腎小管分泌能力 (D) 有效過濾壓 (94 專普一 ) 2. 膀胱逼尿肌收縮而排尿, 主要為透過何種神經之反射而完成? (A) 交感神經 (B)