Renal Physiology
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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. -
Kidney, Renal Tubule – Dilation
Kidney, Renal Tubule – Dilation Figure Legend: Figure 1 Kidney, Renal tubule - Dilation in a male B6C3F1 mouse from a chronic study. Dilated tubules are noted as tracts running through the cortex and outer medulla. Figure 2 Kidney, Renal tubule - Dilation in a male F344/N rat from a chronic study. Tubule dilation is present throughout the outer stripe of the outer medulla, extending into the cortex. Figure 3 Kidney, Renal tubule - Dilation in a male B6C3F1 mouse from a chronic study. Slight tubule dilation is associated with degeneration and necrosis. Figure 4 Kidney, Renal tubule - Dilation in a male F344/N rat from a chronic study. Tubule dilation is associated with chronic progressive nephropathy. Comment: Renal tubule dilation may occur anywhere along the nephron or collecting duct system. It may occur in focal areas or as tracts running along the entire length of kidney sections (Figure 1). 1 Kidney, Renal Tubule – Dilation Renal tubule dilation may occur from xenobiotic administration, secondary mechanisms, or an unknown pathogenesis (see Kidney – Nephropathy, Obstructive (Figure 2). Dilation may result from direct toxic injury to the tubule epithelium interfering with absorption and secretion (Figure 3). It may also occur secondary to renal ischemia or from prolonged diuresis related to drug administration. Secondary mechanisms of tubule dilation may result from lower urinary tract obstruction, the deposition of tubule crystals, interstitial inflammation and/or fibrosis, and chronic progressive nephropathy (Figure 4). A few dilated tubules may be regarded as normal histologic variation. Recommendation: Renal tubule dilation should be diagnosed and given a severity grade. The location of tubule dilation should be included in the diagnosis as a site modifier. -
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. -
L5 6 -Renal Reabsorbation and Secretation [PDF]
Define tubular reabsorption, Identify and describe tubular secretion, Describe tubular secretion mechanism involved in transcellular and paracellular with PAH transport and K+ Glucose reabsorption transport. Identify and describe Identify and describe the Study glucose titration curve mechanisms of tubular characteristic of loop of in terms of renal threshold, transport & Henle, distal convoluted tubular transport maximum, Describe tubular reabsorption tubule and collecting ducts splay, excretion and filtration of sodium and water for reabsorption and secretion Identify the tubular site and Identify the site and describe Revise tubule-glomerular describe how Amino Acids, the influence of aldosterone feedback and describe its HCO -, P0 - and Urea are on reabsorption of Na+ in the physiological importance 3 4 reabsorbed late distal tubules. Mind Map As the glomerular filtrate enters the renal tubules, it flows sequentially through the successive parts of the tubule: The proximal tubule → the loop of Henle(1) → the distal tubule(2) → the collecting tubule → finally ,the collecting duct, before it is excreted as urine. A long this course, some substances are selectively reabsorbed from the tubules back into the blood, whereas others are secreted from the blood into the tubular lumen. The urine represent the sum of three basic renal processes: glomerular filtration, tubular reabsorption, and tubular secretion: Urinary excretion = Glomerular Filtration – Tubular reabsorption + Tubular secretion Mechanisms of cellular transport in the nephron are: Active transport Pinocytosis\ Passive Transport Osmosis “Active transport can move a solute exocytosis against an electrochemical gradient and requires energy derived from metabolism” Water is always reabsorbed by a Simple diffusion passive (nonactive) (Additional reading) Primary active (without carrier physical mechanism Secondary active The proximal tubule, reabsorb protein) called osmosis , transport large molecules such as transport Cl, HCO3-, urea , which means water proteins by pinocytosis. -
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, -
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. -
Claudins in the Renal Collecting Duct
International Journal of Molecular Sciences Review Claudins in the Renal Collecting Duct Janna Leiz 1,2 and Kai M. Schmidt-Ott 1,2,3,* 1 Department of Nephrology and Intensive Care Medicine, Charité-Universitätsmedizin Berlin, 12203 Berlin, Germany; [email protected] 2 Molecular and Translational Kidney Research, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), 13125 Berlin, Germany 3 Berlin Institute of Health (BIH), 10178 Berlin, Germany * Correspondence: [email protected]; Tel.: +49-(0)30-450614671 Received: 22 October 2019; Accepted: 20 December 2019; Published: 28 December 2019 Abstract: The renal collecting duct fine-tunes urinary composition, and thereby, coordinates key physiological processes, such as volume/blood pressure regulation, electrolyte-free water reabsorption, and acid-base homeostasis. The collecting duct epithelium is comprised of a tight epithelial barrier resulting in a strict separation of intraluminal urine and the interstitium. Tight junctions are key players in enforcing this barrier and in regulating paracellular transport of solutes across the epithelium. The features of tight junctions across different epithelia are strongly determined by their molecular composition. Claudins are particularly important structural components of tight junctions because they confer barrier and transport properties. In the collecting duct, a specific set of claudins (Cldn-3, Cldn-4, Cldn-7, Cldn-8) is expressed, and each of these claudins has been implicated in mediating aspects of the specific properties of its tight junction. The functional disruption of individual claudins or of the overall barrier function results in defects of blood pressure and water homeostasis. In this concise review, we provide an overview of the current knowledge on the role of the collecting duct epithelial barrier and of claudins in collecting duct function and pathophysiology. -
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. -
The Urinary System Dr
The urinary System Dr. Ali Ebneshahidi Functions of the Urinary System • Excretion – removal of waste material from the blood plasma and the disposal of this waste in the urine. • Elimination – removal of waste from other organ systems - from digestive system – undigested food, water, salt, ions, and drugs. + - from respiratory system – CO2,H , water, toxins. - from skin – water, NaCl, nitrogenous wastes (urea , uric acid, ammonia, creatinine). • Water balance -- kidney tubules regulate water reabsorption and urine concentration. • regulation of PH, volume, and composition of body fluids. • production of Erythropoietin for hematopoieseis, and renin for blood pressure regulation. Anatomy of the Urinary System Gross anatomy: • kidneys – a pair of bean – shaped organs located retroperitoneally, responsible for blood filtering and urine formation. • Renal capsule – a layer of fibrous connective tissue covering the kidneys. • Renal cortex – outer region of the kidneys where most nephrons is located. • Renal medulla – inner region of the kidneys where some nephrons is located, also where urine is collected to be excreted outward. • Renal calyx – duct – like sections of renal medulla for collecting urine from nephrons and direct urine into renal pelvis. • Renal pyramid – connective tissues in the renal medulla binding various structures together. • Renal pelvis – central urine collecting area of renal medulla. • Hilum (or hilus) – concave notch of kidneys where renal artery, renal vein, urethra, nerves, and lymphatic vessels converge. • Ureter – a tubule that transport urine (mainly by peristalsis) from the kidney to the urinary bladder. • Urinary bladder – a spherical storage organ that contains up to 400 ml of urine. • Urethra – a tubule that excretes urine out of the urinary bladder to the outside, through the urethral orifice. -
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. -
Laboratory 8 - Urinary and Reproductive Systems
Laboratory 8 - Urinary and Reproductive Systems Urinary System Please read before starting: It is easy to damage the structures of the reproductive system as you expose structures associated with excretion, so exercise caution as you do this. Please also note that we will have drawings available as well to help you find and identify the structures described below. The major blood vessels serving the kidneys are the Renal renal artery and the renal pyramid vein., which are located deep in the parietal peritoneum. The renal artery is a branch of the dorsal aorta that comes off Renal further caudal than the cranial pelvis mesenteric artery. Dissect the left kidney in situ, dividing it into dorsal and ventral portions by making a frontal section along the outer periphery. Observe the renal cortex renal medulla (next layer in) renal pyramids renal pelvis ureter (see above diagram) The kidneys include a variety of structures including an arterial supply, a venous return, extensive capillary networks around each nephron and then, of course, the filtration and reabsorption apparatus. These structures are primarily composed of nephrons (the basic functional unit of the kidney) and the ducts which carry urine away from the nephron (the collecting ducts and larger ducts eventually draining these into the ureters from each kidney. The renal pyramids contain the extensions of the nephrons into the renal medulla (the Loops of Henle) and the collecting ducts. Urine is eventually emptied into the renal pelvis before leaving the kidneys in the ureters. The ureters leaves the kidneys medially at approximately the midpoint of the organs and then run caudal to the urinary bladder. -
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.