Urinary concentration and dilution

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1 Urinary concentration and dilution
Concentrative urine浓缩尿: Osmolality of urine > plasma osmolality (300mOsm/L H2O) Diluted urine稀释尿: Osmolality of urine < plasma osmolality

2 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

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

4 The Osmotic Gradient of the Renal Medulla

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

6 Permeability of the Tubular System
H2O NaCl Urea Thin descending limb ++ _ Thick ascending limb Actively transport Thin ascending limb + Distal tubule + ADH Cortical collecting duct Inner medullary collecting duct

7 Formation of Osmotic Gradient of the Renal Medulla
B C Na+ H2O The countercurrent theory 1. Countercurrent multiplication逆流倍增

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9 1.Countercurrent multiplication
Na+ H2O

10 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

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12 The Countercurrent Theory
2. Countercurrent exchange 逆流交换

13 2. Countercurrent exchange

14 Maintenance of the Osmotic Gradient in the Medulla
Vasa recta

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

16 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

17 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

18 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

19 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

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

21 Diabetes Insipidous尿崩症

22 Regulation of ADH Release
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 ↓

23 Water diuresis 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

24 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+

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

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

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

28 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.

29 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.

30 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:

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

32 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

33 Use of Clearance Methods to Quantify Kidney Function
UxV =GF – R + E G=GFR F=Filtration concentration

34 Use of Clearance Methods to Quantify Kidney Function
Inulin clearance as a measure of glomerular filtration

35 Use of Clearance Methods to Quantify Kidney Function
Clearance of para-aminohippuric acid as a measure of renal plasma flow Para-aminohippuric acid (PAH) freely through the glomerulus Almost all the remaining PAH in the plasma is secreted into the tubule

36 Use of Clearance Methods to Quantify Kidney Function
Renal clearance as a calculation of tubular reabsorption or secretion By comparison of inulin clearance with clearances of different solutes  C<125ml／min-----has reabsorption  C>125ml／min-----has secretion

37 Micturition 排尿 Innervation of the bladder and urethra

38 Micturition

39 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

40 Micturition Reflex Micturition occurs when the intravesicular pressure reaches 70 cmH2O via a reflex action Pdet, cm H2O 50 volume ml

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

42 Pathways of Micturition Reflex

43 Micturition 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

44 Micturition reflex

45 Enuresis遗尿

46 Summary Term: Renal clearance
List the factors that affect the concentration and dilution of the urine

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

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

49 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？

50 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。

51 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。

52 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。

53 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80-180mmHg( 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。

54 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+- Na+交换增强，肾排H+增加。③NH3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。

55 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。

56 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。

57 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。

58 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。