肾小管与集合管的重吸收

1、第二节 肾小管与集合管的重吸收 Reabsorption in the renal tubule and collecting duct,超滤液量(ultrafiltrate volume)180L /日 尿量(urine volume)1.5L /日 提示99%被重吸收 1%排出体外 某物质 终尿浓度u / 血浆浓度P 反映物质被重吸收或分泌的情况 因为水的重吸收量达99%，流量缩小了100倍， 所以u/p=100的物质既不被重吸收又不被分泌和排泄 u/p100如肌酐(creatinine)等，提示肾小管还有分泌和排泄功能,重吸收部位,近球小管(proximal tubule) 14mm,刷

2、状缘(brush border)增大重吸收面积 髓袢(Henles loop) 210mm 远球小管(distal tubule) 13.6mm 集合管(collecting duct) 20mm,一、重吸收的方式,1.被动重吸收(passive transport)：指小管液中的水和溶质依借电化学差通过肾小管上皮细胞进入细胞外液的过程。 Water and solutes are transported across the tubular epithelial cells into the extracellular fluid that is mediated by electronic

3、 and chemical forces. 水借渗透压(osmotic forces)之差被动重吸收，渗透压差是其动力。 溶质浓度差(difference of concentration)和电位差(difference of potential)（电化学差）是其被动重吸收的动力,浓度差,电位差,Na,Na,主动,Na,Na,H,2,O,Cl,Cl,_,尿素,尿素被动扩散,2.主动重吸收(active transport)：指肾小管上皮细胞逆电化学差，将小管内溶质主动转运到小管外组织间液的过程。 Active transport can move a solute against an ele

4、ctrochemical gradient and requires energy derived from metabolism. 逆浓度差 逆电位差,髓袢升支粗段(thick segment of ascending limb) 继发性主动转运(secondary active transport) 特点：逆电化学差 耗能 Characteristics: against an electrochemical gradient and requires energy ) 葡萄糖(glucose)、氨基酸(amino acid)、Na+等主动重吸收,二、几种物质的重吸收1. Na+的重吸收,

5、方式主动重吸收(active transport) 原尿(glomerular filtrate) Na+ 500g /日， 终尿(urine) Na+ 35g /日 99%回收 地点和吸收比例： 近球小管：占滤过量6570% 远曲小管：10% 髓袢：20% 集合管：耗O2 1克，重吸收Na+ 2030克主动转运,各段小管重吸收Na+ 的机制 近球小管 Proximal tubule 近球小管前半段： Na+与GS、氨基酸同向转运(symport) 主动重吸收(active transport) Na +与H + 逆向转运(antiport,近球小管后半段： Na+、Cl- 细胞旁路被动重吸收

6、(paracellular pathway,近球小管泵漏模式(pump-leak model,A 首先小管腔Na+顺浓度差扩散入小管细胞内 There is a concentration gradient favoring sodium diffusion into the cell. B 细胞侧膜的钠泵将其泵入细胞间隙 The cell has sodium pump to transport sodium out of the cell into the interstitium. C 水因渗透压被吸引到间隙，造成间隙内静水压升高 Water moves to the interstit

7、ium by osmosis,and it leads to a high level of hydrostatic pressure in interstitium,D 静水压升高引起Na+和水通过基膜进入细胞间液和相邻毛细血管，并有回漏现象. Sodium and water are reabsorbed from the interstitial fluid into the peritubular capillaries by hydrostatic pressure ,meanwhile,there also exits leakage from interstitial fluid

8、 to tubule. E 在Na+被重吸收时，尚有相当量的负离子（HCO3- 或Cl-）顺Na+被重吸收时造成的电位差而被重吸收。 Many negative ions are reabsorbed by difference of potential induced by the process of sodium reabsorption,远曲小管：Na+重吸收量少 A 紧密连接(tight junctions)对Na+通透性低，回漏量少 B 管内外浓度差大，电位差大 20mfT/L : 140mfT/L 管内-1045 mV C 管腔膜(luminal membrane)和管周膜(ba

9、solateral membrane)分布有Na+泵(sodium pump)，可将Na+泵到细胞外液和毛细血管内 D 伴有负离子重吸收和Na+ -H+ 、Na+-K+交换,髓袢(Henles loop)：主动转运与Cl-继发性主动转运(secondary active transport)升支粗段被动转运相结合。 集合管(connecting tubule)：主动转运，Na+重吸收造成管内-35mV。机制未明,2. Cl-的重吸收,大部分是伴随Na+的主动重吸收而被动重吸收。 When sodium is reabsorbed through the tubular epithelial c

10、ell,negative ions such as chloride are transported passively along with sodium. 各段小管重吸收Cl-的机制： 近球小管(proximal tubule)：管内负电位是Na+依赖性,A Na+的主动重吸收形成小管内外电位差，管内-4mV Sodium is positively reabsorbed from the tubule. This creates a difference of potential. B 负离子HCO3-、Cl-顺电位差被动重吸收 Negative ions such as HCO3-、C

11、l- are passively reabsorbed by difference of potential. C HCO3-比Cl-优先重吸收，加上渗透压差导致水的重吸收 小管液中Cl-浓度 Preferential reabsorption of HCO3- and the reabsorption of water by osmosis pressure lead to a high concentration of chloride in tubule. D Cl-的管内外浓度差又造成Cl-被动重吸收 Cl- is reabsorbed passively by the differe

12、nce of concentration,髓袢升支粗段，管腔内正电位（+2+10mV,正电位依赖Cl-、K+存在。 Na+、Cl-、K+由同一载体协同转运。 Movement of sodium across the luminal membrane is mediated primarily by a 1-sodium,2-chloride,1-potassium cotransporter. 用哇巴因(-) 钠泵，转运受阻，提示Na+泵参与此过程，机制可能如下： The transport is blocked by using ouabain which blocks the activ

13、ity of sodium pump,A 升支粗段上皮细胞管周膜的Na+泵将Na+由胞内泵向组织间液 Sodium is transported from the epithelial cell into interstitial fluid by the activity of sodium pump in the epithelial cell basolateral membranes. B Na+被泵出后，细胞内Na+ ，出现管腔内与细胞内Na+浓度差 Sodium pump maintains a low intracellular sodium concentration,C 管腔

14、内Na+顺此浓度差扩散到细胞内，但须与Cl-、K+由同一载体协同转运。Na+:2Cl-:K+ The low intracellular sodium concentration in turn provides a favorable gradient for movement of sodium from the tubular fluid into the cell.In the thick ascending loop,movement of sodium across the luminal membrane is mediated by a 1-sodium,2-chloride,

15、1-potassium cotransporter,D 进入细胞后， Na+经Na+泵泵到组织间液 Na+ is transported to interstitial fluid by sodium pump. Cl-顺浓度差经管周膜扩散到组织间液 Cl- diffuses into interstitial fluid through basolateral membrane. K+由于浓度差经管腔膜返回管腔内 K+ returns to tubule through basolateral membrane by difference of concentration,E 由于Cl-进入

16、组织间液多，K+返回管腔内液多，造成管腔内正电位 特点：Na+主动转运(active transport)，Cl-继发性主动转运(secondary active transport)速尿(furosedon)、利尿酸(-)(crinuryl,3.水的重吸收,99%重吸收，1%排出体外 水的重吸收： 在近球小管重吸收，伴溶质而重吸收，与体内是否缺水无关 In proximal tubule,the reabsorption of water is accompanied with the reabsorption of solutes. 在远曲小管和集合管吸收，吸收量受调节，体内缺少水时重吸收

17、多，体内不缺水时重吸收少。 In distal tubule and collecting duct water reabsorption is regulated by the condition of body,近球小管6570% 水在各段小管 髓袢 10% 重吸收比例 远曲小管 10% 集合管 1020% 近球小管管壁对水通透性高，高远曲小管34倍，是一种等渗重吸收。 In proximal tubule， the process of water reabsorption is isosmotic because the permeability of tubule to water

18、is high. 髓袢、远曲小管集合管对水的重吸收机制，见尿液浓缩与稀释,4. HCO3-的重吸收,特点：肾小管重吸收HCO3-是以CO2的形式而非直接以HCO3-的形式进行，回到血中的HCO3-是由细胞产生，并非小管液中的HCO3-。 HCO3- is reabsorbed as a gas form. HCO3-比Cl-优先重吸收，是因为CO2能迅速透过管腔膜,5.K+的重吸收,滤过液35克/日，终尿24克/日 主细胞重吸收Na+和水, 分泌K+ 。闰细胞则主要分泌H+。 The principal cells reabsorb sodium and water and secrete p

19、otassium; the intercalated cells secrete hydrogen. 特点：滤过液中的K+绝大部分被重吸收（在近球小管），终尿中的K+主要是由远曲小管和集合管分泌。 Almost all potassium in proximal tubule is reabsorbed,and the potassium in urine is mostly secreted by distal tubule and collecting duct. 近球小管管腔内-4mV，K+重吸收逆电位差主动重吸收,6.葡萄糖的重吸收,A 逆浓度差主动重吸收 B 借助Na+的主动重吸收而

20、继发主动重吸收 C 与刷状缘载体蛋白有关，协同转运 D 胞内葡萄糖通过管周膜进入组织间液的过程是易化扩散。 A specific carrier protein in the brush border combines with a sodium ion and a glucose molecule at the same time.The transport mechanism is so efficient that it removes virtually all the glucose from the tubular lumen.After entry into the cell,g

21、lucose exits across the basolateral membranes by facilitated diffusion,driven by the high glucose concentration in the cell,肾糖阈(renal glucose threshold)：当血中葡萄糖浓度160180mg%时，超过部分肾小管重吸收葡萄糖的能力，出现尿糖。 When the concentration of glucose in blood is above 160180mg%,a small amount of glucose begins to appear

22、in the urine. 葡萄糖吸收极限量(transport maximum)：当血糖浓度增高到令全部肾小管对糖重吸收的能力到达极限时，此值叫。（男375mg/min，女300mg/min） The overall transport maximum for the kidneys is reached when all nephrons have reached their maximal capacity to reabsorb glucose. E 如近球小管对Na+重吸收 ，葡萄糖吸收极限量也,7.其它物质重吸收,氨基酸同葡萄糖 HPO4 、SO4与Na+伴联,第三节 肾小管与集合

23、管的分泌和排泄,肾小管分泌(tubular secretion)：指小管上皮细胞通过新陈代谢，将它所产生的物质分泌到小管液中去的过程。 肾小管排泄(tubular excretion) ：指肾小管上皮细胞将血液中某些物质直接排到小管中去的过程,1.H+的分泌,H+的产生： CO2+H2O H2CO3 HCO3 - +H+ H+-Na+交换，方向相反, 叫逆向交换(counter-transport) H+分泌到小管液中，主要在近球小管发生,远曲小管和集合管：除H+ -Na+交换外，还有K+-Na+交换，两者相互抑制，当酸中毒时H+ ，H+-Na+交换加强，K+-Na+交换 ，或造成血K+ ，反

24、过来用乙酰唑胺(-) 碳酸酐酶(carbonic anhydrase)，使H+ 以纠正酸中毒，会使H+-Na+交换 ，K+- Na+交换 ，造成血K+ 。 （临床上应予注意,2.NH3的分泌,远球小管和集合管的上皮细胞在代谢过程中产生NH3 The epithelial cells of the distal tubule and collecting duct produce NH3 during the process of metabolism. 谷氨酰胺（Glutamyl)(脱氢） NH3 扩散到小管液 NH3+H+ NH4,3K+的分泌,来源：尿K+来自远曲小管和集合管的分泌，原尿中

25、的K+ 在近球小管已被重吸收入血。 The potassium ions in urine is secreted by distal tubule and collecting duct,and the potassium ions in ultrafiltrate is reabsorbed into blood in proximal tubule. 特点： K+的分泌是一种被动分泌过程，与Na+- K+交换 有关。 B. Na+主动重吸收，造成管腔内-10-45mV，促使K+ 从组织液扩散入管腔内液,4.其它物质排泄,肌酐（creatinine）、对氨基马尿酸（aminohippura

26、te）既滤过又排泄 青霉素(benzylpenicillin）、酚红(phenolsulfonphthalein）主要是排泄,5.影响肾小管与集合管泌尿机能的因素,1)小管液中溶质的浓度(the concentration of solute in tubule) 溶质浓度 ，渗透压 ，重吸收 。 渗透性利尿(osmotic diuresis)提高小管液溶质浓度，达到利尿 (2)肾小球滤过率(glomerular filtration rate,球管平衡(glomerulotubular balance)： 在近球小管中：GFR ，重吸收率 ；反之亦然 即不管GFR升高或降低，滤液的重吸收率始

27、终占GFR的6570%左右（重吸收率为6570%） One of the most basic mechanisms for controlling tubular reabsorption is the intrinsic ability of the tubules to increase their reabsorption rate in response to increased tubular load.This phenomenon is referred to as glomerulotubular balance.If GFR is increased,the absolut

28、e rate of proximal tubular reabsorption also increases,and the percentage of GFR reabsorbed in the proximal tubular remains relatively constant at about 65-70 percent,机制： a.近球小管对Na+的定比重吸收，对Na+重吸收量是滤过量的6570%. The percentage of GFR reabsorbed in the proximal tubular remains relatively constant at abou

29、t 65-70 percent. b.肾小管重吸收机能对GFR的影响。 重吸收 小管内压 囊内压 有效滤过压 滤过 球管平衡在渗透性利尿(osmotic diuresis)时会被打乱，6570%水肿,第四节 尿液的浓缩和稀释 concentration and dilution of urine,肾脏对尿液的浓缩和稀释能力在调节水平衡方面有极为重要的作用。 一、尿浓缩和稀释的机制逆流学说 （一）逆流倍增与逆流交换 髓袢、集合管结构排列相似于逆流倍增的模型 直小血管的结构排列近似于逆流交换模型,二）逆流学说 用冰点降低法测定肾分层切片的渗透压，发现：皮质部组织液体与血浆是等渗的，髓质部随髓质外层

30、向乳头部深入而逐渐升高，即渗透压由外向内逐步升高，有明确梯度,1.髓质渗透压梯度形成机制the major factors that contribute to the buildup of solutes concentration into the renal medulla are as follows,A.外髓部渗透压梯度主要是由髓袢升支粗段NaCl的重吸收形成的（Na+主动重吸收，Cl-继发性主动重吸收） The main force is active transport of sodium ions and co-transport of potassium,chloride,a

31、nd other ions out of the thick portion of the ascending limb of the loop of Henle into the medullary interstitium. B.内髓部组织间液的渗透压是由内髓部集合管扩散出来的尿素以及升支细段扩散出来的NaCl这两个因素形成. Passive diffusion of large amounts of urea from the inner medullary collecting ducts into the medullary interstitium and NaCl from th

32、in segment of ascending limb,C.髓袢升支粗段对Na+和Cl-的主动重吸收是主要动力，尿素再循环则促成了整个髓质渗透压梯度的建立。 The main force is the active transport of sodium ions and chloride ions in thick portion of the ascending limb of the loop of Henle ,and urea recirculation also contributes to the whole hyperosmotic renal medullary inter

33、stitium,1.髓质渗透压梯度形成机制,D. 远曲小管及皮质部和外髓部的集合管对尿素不易通透, 水被重吸收, 小管液中尿素的浓度逐渐升高。 In distal tubule and collecting duct, there is little permeability to urea ,and water is reabsorbed ,so that the concentration of urea rises gradually. E. 髓袢降支细段对尿素及Na+都不易通透, 对水易通透, 水被“抽吸”出来, 小管液被浓缩，其中尿素及Na+的浓度不断升高。 Becasuse there is a high permeability to water and l