L5 6 -Renal Reabsorbation and Secretation [PDF]
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Relationship Between Energy Requirements for Na+Reabsorption
Kidney international, Vol. 29 (1986), pp. 32—40 Relationship between energy requirements for Na reabsorption and other renal functions JULIUS J. COHEN Department of Physiology, University of Rochester, Rochester, New York, USA In the intact organism, while the kidney is only —1% of totalkidney in that: (I) Na transport is inhibited by amiloride [7, 81 body weight, it utilizes approximately 10% of the whole bodyand (2) only a small fraction (5 to 10%) of the Na transported 02 consumption (Q-02).Becausethere is a linear relationshipfrom the mucosal to serosal side leaks back to the inucosal side between change in Na reabsorption and suprabasal renal 02[7, 81. In such a tight epithelium, net Na flux is therefore a consumption, the high suprabasal renal Q-02 has been attrib-close approximation of the unidirectional active Na flux. If no uted principally to the energy requirements for reabsorption ofother energy-requiring functions are changed when Na trans- the filtered load of Na [1—31. The basal metabolism is theport is varied, then a reasonable estimate of the energy require- energy which is required for the maintenance of the renal tissuement for both net and unidirectional active Na transport may integrity and turnover of its constituents without measurablebe obtained from measurements of the ratio, Anet T-Na5/AQ- external (net transport or net synthetic) work being done.02. However, there is now considerable evidence that there are Assuming that 3 moles of ADP are phosphorylated to form other suprabasal functions of the kidney which change inATP per atom of 02 reduced in the aerobic oxidation of I mole parallel with Na reabsorption and which require an energyof NADH by the mitochondrial electron transport chain (that is, input separate from that used for Na transport. -
Control of Fluid Absorption in the Renal Proximal Tubule
Control of fluid absorption in the renal proximal tubule Maurice B. Burg, Jack Orloff J Clin Invest. 1968;47(9):2016-2024. https://doi.org/10.1172/JCI105888. Research Article Glomerulotubular balance was investigated in isolated, perfused rabbit proximal tubules in vitro in order to evaluate some of the mechanisms proposed to account for the proportionate relationship between glomerular filtration rate and fluid absorption generally observed in vivo. The rate of fluid transport from lumen to bath in proximal convoluted tubules in vitro was approximately equal to the estimated normal rate in vivo. The absorption rate in proximal straight tubules however was approximately one-half as great. If the mechanism responsible for maintenance of glomerulotubular balance is intrinsic to the proximal tubule, as has been proposed on the basis of micropuncture studies, the rate of fluid absorption in vitro should be directly related to the perfusion rate and/or tubule volume. In the present studies absorption rate was only minimally affected when perfusion rate was increased or the tubule distended. Thus, glomerulotubular balance is not mediated by changes in velocity of flow of the tubular fluid or tubular diameter and therefore is not an intrinsic property of the proximal tubule. It has also been proposed that glomerulotubular balance results from a humoral feedback mechanism in which angiotensin directly inhibits fluid absorption by the proximal convoluted tubule. In the present experiments, angiotensin was found to have no significant effect on absorption rate. Find the latest version: https://jci.me/105888/pdf Control of Fluid Absorption in the Renal Proximal Tubule MAURICE B. -
Kidney Questions
Kidney Questions Maximum Mark Question Mark Awarded 1 12 2 11 3 14 4 12 5 15 6 15 7 16 8 16 9 14 10 14 11 18 Total Mark Page 1 of 44 | WJEC/CBAC 2017 pdfcrowd.com 1. Page 2 of 44 | WJEC/CBAC 2017 pdfcrowd.com Page 3 of 44 | WJEC/CBAC 2017 pdfcrowd.com 2. Roughly 60% of the mass of the body is water and despite wide variation in the quantity of water taken in each day, body water content remains incredibly stable. One hormone responsible for this homeostatic control is antidiuretic hormone (ADH). (a) Describe the mechanisms that are triggered in the mammalian body when water intake is reduced. [6] (b) The graph below shows how the plasma concentration of antidiuretic hormone changes as plasma solute concentration rises. (i) Describe the relationship shown in the graph opposite. Page 4 of 44 | WJEC/CBAC 2017 pdfcrowd.com [2] (ii) Suggest why a person only begins to feel thirsty at a plasma solute concentration of 293 AU. [2] Secretion of antidiuretic hormone is stimulated by decreases in blood pressure and volume. These are conditions sensed by stretch receptors in the heart and large arteries. Severe diarrhoea is one condition which stimulates ADH secretion. (c) Suggest another condition which might stimulate ADH secretion. [1] Page 5 of 44 | WJEC/CBAC 2017 pdfcrowd.com 3. The diagram below shows a single nephron, with its blood supply, from a kidney. (a) (i) Name A, B and C shown on the diagram above. [3] A . B . C . (ii) Use two arrows, clearly labelled, on the nephron above, to show where the following processes take place: [2] I ultrafiltration; Page 6 of 44 | WJEC/CBAC 2017 pdfcrowd.com II selective reabsorption. -
Ludwig's Theory of Tubular Reabsorption: the Role of Physical Factors in Tubular Reabsorption
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 9 (1976) p. 313—322 EDITORIAL REVIEW Ludwig's theory of tubular reabsorption: The role of physical factors in tubular reabsorption From the very origins of physiology as a science, chet [2] created a sensation among physiologists and interest was focused on flow of body fluids. Beginning physicians alike. Quoting from a review [3], appear- with movement of fluid inside blood vessels and later ing in 1828 in the first volume of the American Jour- extending to that across membranes, physiologists nal of Medical Science, of Dutrochet's experiments: have sought mechanical explanations for these phe- "M. Dutrochet has recently published a work on vital nomena. The action of physicochemical forces across motion, in which he details experiments and discov- endothelial membrane structures is reasonably well eries, of a most interesting and extraordinary char- understood, at least in a qualitative sense; it is essen- acter, calculated to throw a new light upon an tially the same as for certain collodion membranes. important portion of physiology. ... M.Dutrochet On the other hand, there is as yet no general con- was, as yet, unable to assign a cause for this physico- sensus regarding the means by which physicochemical organic phenomenon, to which he applied the name forces influence convective flux (volume flux) across of endosmose." It appears to have been Graham who epithelial membranes. In fact, -
Vocabulario De Morfoloxía, Anatomía E Citoloxía Veterinaria
Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) Servizo de Normalización Lingüística Universidade de Santiago de Compostela COLECCIÓN VOCABULARIOS TEMÁTICOS N.º 4 SERVIZO DE NORMALIZACIÓN LINGÜÍSTICA Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) 2008 UNIVERSIDADE DE SANTIAGO DE COMPOSTELA VOCABULARIO de morfoloxía, anatomía e citoloxía veterinaria : (galego-español- inglés) / coordinador Xusto A. Rodríguez Río, Servizo de Normalización Lingüística ; autores Matilde Lombardero Fernández ... [et al.]. – Santiago de Compostela : Universidade de Santiago de Compostela, Servizo de Publicacións e Intercambio Científico, 2008. – 369 p. ; 21 cm. – (Vocabularios temáticos ; 4). - D.L. C 2458-2008. – ISBN 978-84-9887-018-3 1.Medicina �������������������������������������������������������������������������veterinaria-Diccionarios�������������������������������������������������. 2.Galego (Lingua)-Glosarios, vocabularios, etc. políglotas. I.Lombardero Fernández, Matilde. II.Rodríguez Rio, Xusto A. coord. III. Universidade de Santiago de Compostela. Servizo de Normalización Lingüística, coord. IV.Universidade de Santiago de Compostela. Servizo de Publicacións e Intercambio Científico, ed. V.Serie. 591.4(038)=699=60=20 Coordinador Xusto A. Rodríguez Río (Área de Terminoloxía. Servizo de Normalización Lingüística. Universidade de Santiago de Compostela) Autoras/res Matilde Lombardero Fernández (doutora en Veterinaria e profesora do Departamento de Anatomía e Produción Animal. -
Excretory Products and Their Elimination
290 BIOLOGY CHAPTER 19 EXCRETORY PRODUCTS AND THEIR ELIMINATION 19.1 Human Animals accumulate ammonia, urea, uric acid, carbon dioxide, water Excretory and ions like Na+, K+, Cl–, phosphate, sulphate, etc., either by metabolic System activities or by other means like excess ingestion. These substances have to be removed totally or partially. In this chapter, you will learn the 19.2 Urine Formation mechanisms of elimination of these substances with special emphasis on 19.3 Function of the common nitrogenous wastes. Ammonia, urea and uric acid are the major Tubules forms of nitrogenous wastes excreted by the animals. Ammonia is the most toxic form and requires large amount of water for its elimination, 19.4 Mechanism of whereas uric acid, being the least toxic, can be removed with a minimum Concentration of loss of water. the Filtrate The process of excreting ammonia is Ammonotelism. Many bony fishes, 19.5 Regulation of aquatic amphibians and aquatic insects are ammonotelic in nature. Kidney Function Ammonia, as it is readily soluble, is generally excreted by diffusion across 19.6 Micturition body surfaces or through gill surfaces (in fish) as ammonium ions. Kidneys do not play any significant role in its removal. Terrestrial adaptation 19.7 Role of other necessitated the production of lesser toxic nitrogenous wastes like urea Organs in and uric acid for conservation of water. Mammals, many terrestrial Excretion amphibians and marine fishes mainly excrete urea and are called ureotelic 19.8 Disorders of the animals. Ammonia produced by metabolism is converted into urea in the Excretory liver of these animals and released into the blood which is filtered and System excreted out by the kidneys. -
Novel Tubular–Glomerular Interplay in Diabetic Kidney Disease Mediated
Clinical and Experimental Nephrology https://doi.org/10.1007/s10157-019-01719-4 INVITED REVIEW ARTICLE Novel tubular–glomerular interplay in diabetic kidney disease mediated by sirtuin 1, nicotinamide mononucleotide, and nicotinamide adenine dinucleotide Oshima Award Address 2017 Kazuhiro Hasegawa1 Received: 6 December 2018 / Accepted: 15 February 2019 © The Author(s) 2019 Abstract Tubules interact with glomeruli, which are composed of podocytes, parietal epithelial cells, mesangial cells, and glomerular endothelial cells. Glomerular–tubular balance and tubuloglomerular feedback are the two components of the tubular–glo- merular interplay, which has been demonstrated to play roles in physiological renal function and in diabetic kidney disease (DKD), in which proteins leaking from glomeruli arrive at tubular regions, leading to further tubular injury caused by the accumulation of proteinuria-inducing reactive oxygens species and various cytokines. In the current review, we present our recent work identifying a novel tubular–glomerular interplay in DKD mediated by sirtuin 1 and nicotinamide mononucleotide. Keywords Sirtuin 1 · Tubuloglomerular feedback · Diabetic kidney disease · Nicotinamide mononucleotide Introduction The longevity gene sirtuin 1 In this review, we summarize our studies revealing the novel We have demonstrated the role of SIRT1 in kidneys, par- roles of sirtuin 1 (SIRT1) and nicotinamide mononucleo- ticularly in DKD. Figure 1 outlines the basic characteristics tide (NMN) in the tubular–glomerular interplay in diabetic of SIRT1, one of the seven isoforms of mammalian sirtuins, kidney disease (DKD). First, we overview the basic func- which are found in specific intracellular compartments. tions of SIRT1 and NMN and changes i1 and NMN during The first sirtuin that was discovered was Sir2 in yeast [1]. -
Glomerular Filtration I DR.CHARUSHILA RUKADIKAR Assistant Professor Physiology GFR 1
Glomerular filtration I DR.CHARUSHILA RUKADIKAR Assistant Professor Physiology GFR 1. Definition 2. Normal value 3. Variation 4. Calculation (different pressures acting on glomerular membrane) 5. Factors affecting GFR 6. Regulation of GFR 7. Measurement of GFR QUESTIONS LONG QUESTION 1. GFR 2. RENIN ANGIOTENSIN SYSTEM SHORT NOTE 1. DYNAMICS OF GFR 2. FILTRATION FRACTION 3. ANGIOTENSIN II 4. FACTORS AFFECTING GLOMERULAR FILTRATION RATE 5. REGULATION OF GFR 6. RENAL CLEARANCE TEST 7. MEASUREMENT OF GFR Collecting duct epithelium P Cells – Tall, predominant, have few organelles, Na reabsorption & vasopressin stimulated water reabsorption I cells- CT and DCT, less, having more cell organelles, Acid secretion and HCO3 transport CHARACTERISTICS OF RENAL BLOOD FLOW 600-1200 ml/min (high) AV O2 difference low (1.5 mL/dL) During exercise increases 1.5 times Low basal tone, not altered in denervated / innervated kidney VO2 in kidneys is directly proportional to RBF, Na reabsorption & GFR Not homogenous flow, cortex more & medulla less Vasa recta hairpin bend like structure, hyperosmolarity inner medulla Transplanted kidney- cortical blood flow show autoregulation & medullary blood flow don’t show autoregulation, so no TGF mechanism Neurogenic vasodilation not exist 20% of resting cardiac output, while the two kidneys make < 0.5% of total body weight. Excretory function rather than its metabolic requirement. Remarkable constancy due to autoregulation. Processes concerned with urine formation. 1. Glomerular filtration, 2. Tubular reabsorption and 3. Tubular secretion. • Filtration Fluid is squeezed out of glomerular capillary bed • Reabsorption Most nutrients, water and essential ions are returned to blood of peritubular capillaries • Secretion Moves additional undesirable molecules into tubule from blood of peritubular capillaries Glomerular filtration Glomerular filtration refers to process of ultrafiltration of plasma from glomerular capillaries into the Bowman’s capsule. -
Nomina Histologica Veterinaria, First Edition
NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria. -
Urea and Renal Function in the 21St Century: Insights from Knockout Mice
Review Urea and Renal Function in the 21st Century: Insights from Knockout Mice Robert A. Fenton* and Mark A. Knepper† *Water and Salt Research Center, Institute of Anatomy, University of Aarhus, Aarhus, Denmark; and †Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institutes, National Institutes of Health, Bethesda, Maryland Since the turn of the 21st century, gene knockout mice have been created for all major urea transporters that are expressed in the kidney: the collecting duct urea transporters UT-A1 and UT-A3, the descending thin limb isoform UT-A2, and the descending vasa recta isoform UT-B. This article discusses the new insights that the results from studies in these mice have produced in the understanding of the role of urea in the urinary concentrating mechanism and kidney function. Following is a summary of the major findings: (1) Urea accumulation in the inner medullary interstitium depends on rapid transport of urea from the inner medullary collecting duct (IMCD) lumen via UT-A1 and/or UT-A3; (2) as proposed by Robert Berliner and colleagues in the 1950s, the role of IMCD urea transporters in water conservation is to prevent a urea-induced osmotic diuresis; (3) the absence of IMCD urea transport does not prevent the concentration of NaCl in the inner medulla, contrary to what would be predicted from the passive countercurrent multiplier mechanism in the form proposed by Kokko and Rector and Stephenson; (4) deletion of UT-B (vasa recta isoform) has a much greater effect on urinary concentration than deletion of UT-A2 (descending limb isoform), suggesting that the recycling of urea between the vasa recta and the renal tubules quantitatively is less important than classic countercurrent exchange; and (5) urea reabsorption from the IMCD and the process of urea recycling are not important elements of the mechanism of protein-induced increases in GFR. -
Prime Mover and Key Therapeutic Target in Diabetic Kidney Disease
Diabetes Volume 66, April 2017 791 Richard E. Gilbert Proximal Tubulopathy: Prime Mover and Key Therapeutic Target in Diabetic Kidney Disease Diabetes 2017;66:791–800 | DOI: 10.2337/db16-0796 The current view of diabetic kidney disease, based on estimated glomerular filtration rate (eGFR) decline (2). In meticulously acquired ultrastructural morphometry and recognition of these findings, the term diabetic kidney the utility of measuring plasma creatinine and urinary al- disease rather than diabetic nephropathy is now commonly bumin, has been almost entirely focused on the glomer- used. On the background of recent advances in the role of ulus. While clearly of great importance, changes in the the proximal tubule as a prime mover in diabetic kidney PERSPECTIVES IN DIABETES glomerulus are not the major determinant of renal prog- pathology, this review highlights key recent developments. nosis in diabetes and may not be the primary event in the Published mostly in the general scientific and kidney- development of diabetic kidney disease either. Indeed, specific literature, these advances highlight the pivotal advances in biomarker discovery and a greater appreci- role this part of the nephron plays in the initiation, pro- ation of tubulointerstitial histopathology and the role of gression, staging, and therapeutic intervention in diabetic tubular hypoxia in the pathogenesis of chronic kidney kidney disease. From a pathogenetic perspective, as illus- disease have given us pause to reconsider the current trated in Fig. 1 and as elaborated on further in this review, “glomerulocentric” paradigm and focus attention on the proximal tubule that by virtue of the high energy require- tubular hypoxia as a consequence of increased energy de- ments and reliance on aerobic metabolism render it par- mands and reduced perfusion combine with nonhypoxia- ticularly susceptible to the derangements of the diabetic related forces to drive the development of tubular atrophy fi state. -
PGE2 EP1 Receptor Inhibits Vasopressin-Dependent Water
Laboratory Investigation (2018) 98, 360–370 © 2018 USCAP, Inc All rights reserved 0023-6837/18 PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct Rania Nasrallah1, Joseph Zimpelmann1, David Eckert1, Jamie Ghossein1, Sean Geddes1, Jean-Claude Beique1, Jean-Francois Thibodeau1, Chris R J Kennedy1,2, Kevin D Burns1,2 and Richard L Hébert1 PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1 − / − mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1 − / − , Htn, HtnEP1 − / − . Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1 − / − , but sglt2 was increased in EP1 − / − mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1 − / − or HtnEP1 − / − mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.