essay questions on renal physiology

The Normal Anatomy and Physiology of the Kidneys: Urine Formation Essay

The external anatomy of kidney, the internal anatomy of kidney, physiological balancing in the nephron.

Kidneys are the major organs of the renal system which perform vital homeostatic processes such as maintenance of water and ionic balance in the body. The kidneys’ primary function is waste removal through ultrafiltration, leading to urine formation. Moreover, they are actively involved in the reabsorption of amino acids, glucose, and water to achieve osmotic balance in the body (Wingerd & Taylor, 2020). In addition, hormones and enzymes are produced from the kidneys, stimulating, and catalysing physiological reactions in the body to achieve homeostasis.

A normal kidney is a brown organ, which has the shape of a bean seed. Each kidney is protected by a cushion called the renal capsule, a fibrous membrane having an irregular network of connecting tissue. The capsule is essential in holding kidneys in their positions within the abdominal cavity (Wingerd & Taylor, 2020). Moreover, it assists in maintaining the shape and responsible for protecting them from mechanical shock. The capsule is also overlayed by the renal fat pad, enhancing its efficacy in reducing the physical impact on the kidneys from an external force. The adipose tissues forming the fat pad are linked to the renal fascia, which in conjunction with the peritoneum, serves as anchorage surfaces for the kidneys to the posterior side of the abdominal cavity (Hickling et al., 2017). The hilum forms the entry point through which renal arteries and veins, and ureters serve the kidneys with fluids flowing in and out.

On top of the kidney is embedded an adrenal gland, which is responsible for modulating the organ’s physiological functions. However, the adrenal glands are part of the endocrine and not the renal system. The anterior interests of kidneys are protected by ribcages that curve into the lumbar region (Hickling et al., 2017). Kidneys are served by blood from the renal artery, which branches from the posterior side of the aorta. The flowing blood from the kidney is channelled into the inferior vena cava through the renal vein (Wingerd & Taylor, 2020). The excretory waste constituting the urine flows from the kidney into the bladder through the ureter. Thus, kidney serves in the purification of blood during the process of urine formation.

The kidney comprises three primary internal layers: the cortex, medulla, and pelvis. The renal cortex is the region immediately after the capsule, and within it are the extended sections of the nephron to form the Bowman’s capsule (Lawrence et al., 2018). It is a granular tissue within the kidney, offering a space for the arterioles and venules emerging from the arteries and veins, respectively. Moreover, the glomerular capillaries, which permit filtration of the blood components, are embedded in the cortex (Wingerd & Taylor, 2020). It is in the renal cortex where erythropoietin hormone is secreted to stimulate erythrocyte formation.

The medulla is the parenchymatous region within the kidney, constituting the immediate layer after the cortex. It is composed of stacked masses of tissue defined as renal pyramids. Each pyramid is comprised of densely interwoven nephrons (Wingerd & Taylor, 2020). The basic unit by which a kidney executes homeostatic function is the nephron. The Bowman capsule located in the cortex connects to the proximal convoluted tubules through which the glomerular filtered plasma flows (Hickling et al., 2017). In the medulla pyramids, the loop of Henle and the distal convoluted tubules form part of the nephron channelling the purified plasma into the collecting ducts.

The renal pelvis is the innermost concaved region of the kidney. Every pyramid of the medulla ends in a renal papilla that supplies concentrated urine into the minor calyces. The pool formed by minor calyces from every renal pyramid constitutes the major calyx. All the significant calyces are consecrated into a single unit called the pelvis (Wingerd & Taylor, 2020). The pelvis connects the kidney to the ureter, thus directing the concentrated urine into the bladder.

The Blood Supply Network

Kidneys are highly vascularized organs, receiving a quarter of the blood circulating within the body at a specific duration of time. The entry of blood into the two kidneys occurs via a pair of renal arteries extending from the aorta. On reaching the hilum of each kidney, the blood is channelled into segmental arteries, which branch into the interlobar arteries (Hickling et al., 2017). The interlobar vessels pass through the columns get into the cortex, in which they branch to form arcuate arteries. Further branching of the blood vessels leads to cortical radiate arteries, which supply their contents into the arterioles. Blood from the arterioles enters the glomerulus via the afferent arteriole. After glomerular filtration, the blood leaves the network of capillaries via the efferent arteriole (McDonald, 2019). Moreover, a portal of blood vessels extends from the afferent and efferent arterioles surrounding the proximal convoluted tubules, the loop of Henle, and the distal convoluted tubule to aid the urine concentration process.

Ultrafiltration in the Glomerulus

The formation of urine begins with the filtration process, which takes place in the glomerulus, a mesh of capillaries connected to the Bowman’s capsule. Ultrafiltration in the glomerulus does not require energy. However, it is accomplished through pressure build-up, which pushes the plasma and solute particles through the capillary walls. The process of filtration is aided through a three-layered membrane system (Lawrence et al., 2018). The fenestrated endothelia of capillaries in the permits plasma to pass through them, and not blood cells. Immediately, the negatively charged basement membrane blocks proteins from passing. Finally, the capsule of the capsule in the glomeruli develops a barrier that allows for the selected particles’ filtration. The efficiency of the filtration process is determined by the pressure create by the cardiac pumps of blood through the aorta, arteries, arterioles, and capillaries (Hickling et al., 2017). The net force for filtration generated in the glomeruli yields the glomerular filtrate channelled into the proximal convoluted tubule via the Bowman’s capsule.

Urine Concentration through Water and Ion Re-absorption

The kidney nephron is characterized by four tubular components in which reabsorption of water, ions, amino acids, and glucose takes place. The proximal convoluted tubule is attributed to the highest capacity of absorbing elements of the glomerular filtrate. From its lumen, sodium ions are taken back to the bloodstream by an active transport mechanism involving basolateral pumping of sodium-potassium ions (Lawrence et al., 2018). The secondary dynamic transport mechanism is involved in the reabsorption of amino acids, glucose, and vitamins. Moreover, water is reabsorbed by osmosis created by the ionic imbalance, which in turn drives the diffusion of lipids across the wall of proximal convoluted tubule into the bloodstream (Gupta & Sharma, 2020). The reabsorption of ions, sugar, amino acids, and lipids is essential in osmoregulation all over the body.

The glomerular filtrate moves into the loop of Henle, having the ascending and descending sections. The reabsorption of water through osmosis into the bloodstream main occurs in the descending spiral. On the other hand, potassium, sodium, and chloride ions are taken back to the bloodstream via the ascending loop of Henle (McDonald, 2019). The ATPase enzyme drives the process by creating an ionic gradient which makes the basolateral membrane of the symporter in the ascending loop to be functional in absorbing ions. Immediately after the loop of Henle, the filtrate enters the distal convoluted tubule where sodium ion absorption occurs. Mainly, active transport is involved in sodium-ion uptake via basolateral membrane (Lawrence et al., 2018). However, its passive absorption into the bloodstream occurs through sodium and chloride ion symporter on the apical plasmalemma. In the distal convoluted tubule, aldosterone hormone regulates sodium ion intake while parathyroid hormone controls the reabsorption of calcium ion (McDonald, 2019). Eventually, concentrated urine remaining in the lumen of the tubules moves into the collecting ducts, where final reabsorption occurs via active transport.

The concentrated urine is channelled into the pelvis; after that, it travels to the urinary bladder via the ureter. The kidney has two major homeostatic roles in the body, that is, maintenance of pH through balancing hydrogen ion concentration and osmoregulation. Moreover, it aids the purification of the blood by removing excess water, salts, and impurities. Its physiological functions encompass energy and the regulated hormonal process leading to the reabsorption of ions into the bloodstream. Thus, the structural and physiological function of the kidney allows urine formation and purification of blood.

Gupta, R., & Sharma, T. (2020). Review of urine formation in Ayurveda. Journal of Ayurveda and Integrated Medical Sciences, 5 (1), 145-148.

Hickling, D. R., Sun, T. T., & Wu, X. R. (2017). Anatomy and physiology of the urinary tract: relation to host defence and microbial infection . In Urinary Tract Infections: Molecular Pathogenesis and Clinical Management (pp. 1-25).

Lawrence, E. A., Doherty, D., & Dhanda, R. (2018). Function of the nephron and the formation of urine . Anaesthesia and Intensive Care Medicine, 19 (5), 249-253.

McDonald, M. D. (2019). The renal contribution to salt and water balance. In Fish Osmoregulation (pp. 309-331). CRC Press.

Wingerd, B., & Taylor, T. B. (2020). The Human Body: Concepts of Anatomy and Physiology . Jones & Bartlett Learning.

• The Mechanisms of Kidney Function
• Pathophysiologic Alterations of the Renal and Urologic Systems
• Kidney Function Tests: Chemical Methods Used to Diagnose Kidney Disease
• Lumbar Disk Herniation: Medical Analysis
• Intracranial Pressure Anatomy
• Physiotherapy and Fractured Neck of Femur
• Motor Skills Development of Young Children
• Rheumatoid Arthritis: Causes, Symptoms, Treatments
• Chicago (A-D)
• Chicago (N-B)

IvyPanda. (2021, October 21). The Normal Anatomy and Physiology of the Kidneys: Urine Formation. https://ivypanda.com/essays/the-normal-anatomy-and-physiology-of-the-kidneys-urine-formation/

"The Normal Anatomy and Physiology of the Kidneys: Urine Formation." IvyPanda , 21 Oct. 2021, ivypanda.com/essays/the-normal-anatomy-and-physiology-of-the-kidneys-urine-formation/.

IvyPanda . (2021) 'The Normal Anatomy and Physiology of the Kidneys: Urine Formation'. 21 October.

IvyPanda . 2021. "The Normal Anatomy and Physiology of the Kidneys: Urine Formation." October 21, 2021. https://ivypanda.com/essays/the-normal-anatomy-and-physiology-of-the-kidneys-urine-formation/.

1. IvyPanda . "The Normal Anatomy and Physiology of the Kidneys: Urine Formation." October 21, 2021. https://ivypanda.com/essays/the-normal-anatomy-and-physiology-of-the-kidneys-urine-formation/.

Bibliography

IvyPanda . "The Normal Anatomy and Physiology of the Kidneys: Urine Formation." October 21, 2021. https://ivypanda.com/essays/the-normal-anatomy-and-physiology-of-the-kidneys-urine-formation/.

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android . Learn more here!

• Remote Access
• Save figures into PowerPoint
• Download tables as PDFs

Questions and Answers

• Download Chapter PDF

Disclaimer: These citations have been automatically generated based on the information we have and it may not be 100% accurate. Please consult the latest official manual style if you have any questions regarding the format accuracy.

Download citation file:

• Search Book

Jump to a Section

• Full Chapter
• Supplementary Content

Please find Review Questions for this title here.

Sign in or create a free Access profile below to access even more exclusive content.

With an Access profile, you can save and manage favorites from your personal dashboard, complete case quizzes, review Q&A, and take these feature on the go with our Access app.

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.

Please Wait

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• Clin J Am Soc Nephrol
• v.9(4); 2014 Apr 7

Defining Kidney Biology to Understand Renal Disease

Melissa h. little.

* Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland, Australia;

Dennis Brown

† Center for Systems Biology and Program in Membrane Biology, and Division of Nephrology, Massachussetts General Hospital, Harvard University, Boston, Massachusetts;

Benjamin D. Humphreys

‡ Renal Division, Brigham and Women's Hospital, Harvard University, Boston, Massachusetts;

Andrew P. McMahon

§ Stem Cell Biology and Regenerative Medicine, University of Southern California, Los Angeles, California;

Jeffrey H. Miner

‖ Renal Division, Washington University School of Medicine, Washington University in St. Louis, St. Louis, Missouri;

Jeff M. Sands

¶ Departments of Medicine and Physiology, Emory University School of Medicine, Atlanta, Georgia;

Ora A. Weisz

** Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; and

Chris Mullins

†† National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland

Deborah Hoshizaki

The Kidney Research National Dialogue represents a novel effort by the National Institute of Diabetes and Digestive and Kidney Diseases to solicit and prioritize research objectives from the renal research and clinical communities. The present commentary highlights selected scientific opportunities specific to the study of renal development, physiology, and cell biology. Describing such fundamental kidney biology serves as a necessary foundation for translational and clinical studies that will advance disease care and prevention. It is intended that these objectives foster and focus scientific efforts in these areas in the coming decade and beyond.

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) recently asked the community to identify research objectives, which, if addressed, would improve our understanding of basic kidney function and aid in the prevention, treatment, and reversal of kidney disease. The Kidney Research National Dialogue (KRND) welcomed all interested parties to submit, discuss, and prioritize ideas through an interactive website ( 1 ). Over 1600 participants posted ideas covering all areas of kidney disease. This commentary represents one important component of the KRND and highlights selected scientific opportunities for studies of renal development, physiology, and cell biology that are expected to provide important contributions to maintaining and improving kidney health and regenerating kidney tissues.

Renal research has undergone a decade-long shift from the study of fundamental kidney biology to the study of renal pathophysiology and translational development of treatment strategies for renal disease. This evolution may have been driven by the perception that continued description of basic kidney biology is unlikely to have direct impact on clinical management of kidney disease. However, the study of kidney biology remains the foundation for understanding renal disease and serves as an engine for driving translational and clinical advances.

There are many examples of fundamental research insights leading to improved patient care. Perhaps the most striking is the molecular characterization of the renin-angiotensin system leading to the development of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for the treatment of renal and cardiovascular disease. Understanding the biology of water reabsorption provided a foundation for the vasopressin-receptor antagonist treatment of hyponatremia and, perhaps, polycystic kidney disease. Cellular signaling studies have identified targets ranging from Nrf2 to Jak/Stat that are currently being tested in human studies. Hence, understanding basic kidney biology remains central to advancing health and driving discoveries for translation to clinical progress in the next decade and beyond. It is clear from these studies that many interrelated factors contribute to normal biology and the progression over time to the development of pathophysiology ( Figure 1 ). Below are a number of fruitful areas of investigation identified in the KRND.

Untangling the knot. Schematic representation of the influence of interrelated environmental and biologic considerations over the life history of the kidney that underlie kidney health.

Renal Embryogenesis

Recent studies have advanced our understanding of renal embryogenesis from the identification of molecular subcompartments and genetic circuitries of developing renal structures to the mechanism of uretic bud branching to the identification of the Six2-expressing cap mesenchyme as the multipotent nephron progenitor population. The next critical step is to place the genetic and cellular basis of renal development in a wider context, which includes the determination of kidney endowment/number of nephrons and reaching out to neglected topics (such as the innervation of the kidney), the patterning of the two major circulatory systems (blood/vascular and lymphatic), the differentiation of the tubular segments, and the regional, functional, and anatomic heterogeneity of nephrons within the kidney. Advances in these topics may allow generation of a functional nephron (with correct vascular, tubular, and neural integration) that will improve kidney function and serve as a foundation for novel physiologic and tissue regeneration studies. They will also underpin potential advances in bioengineering and nephrotoxicity screening.

Environmental Effects

A suboptimal prenatal environment, including placental insufficiency, maternal undernutrition, and glucocorticoid exposure, reduces nephron number and can increase the risk of diseases, including hypertension and hydronephrosis, in offspring. However, the underlying mechanisms by which these factors affect fetal programming and reduce nephron number and kidney efficiency are unknown. To fully understand fetal reprogramming of the kidney and the regulation of kidney size, we will require additional advances in our ability to image and accurately quantitate the size of individual cellular compartments during development as well as quantify nephron number in vivo . Given the relevance of in utero challenge to the community, we also need to apply advanced genetics and epigenetics to the analysis of animal models of fetal environmental perturbation.

Renal Physiology and Cell Biology

It is clear that defining normal physiology and cellular function drives additional discovery and informs clinical management. Over the past several years, our understanding of renal cell function has taken advantage of progress in several fields, including, but not limited to, ion channel and transporters, cell matrix interactions, receptor biology, and signaling cascades. The advent of genetically engineered animals offers exciting opportunities to understand the physiologic effect of over- or underexpression of such proteins in renal function, including those proteins that are mutated in human diseases. Such functional studies provide unique data and the ability to test novel therapeutics for both beneficial effects and unanticipated negative effects. Understanding the pathways and mechanisms that govern sorting and trafficking of proteins essential for kidney function will inform therapeutic strategies for kidney disorders caused by mutations in individual proteins. The use of diverse model systems and humanized mice offers tremendous opportunities, including contributions of cellular mediators to organ physiology. New renal cellular models can elucidate the signaling pathways regulating transport and explore mechanisms, such as protein–protein interactions, protein phosphorylation, protein trafficking, and the role of degradation pathways (ubiquitination and lysosomal degradation). As one example, studies of the primary cilium, whether in algae, zebrafish, or mammals, have led to important insights into polycystic kidney disease and nephronophthisis.

Systems Biology

There has been an explosion of new genetic, proteomic, and imaging techniques applicable to analysis at the organ, cell, or biochemical level. A better grasp is needed of how regulatory mechanisms (like ubiquitination, sumoylation, DNA methylation, histone modifications, and noncoding RNAs) modulate kidney cell functions. Opportunities exist in kidney research for integrating genotype, RNA expression, promoter analysis, proteome expression, and metabolic profiles to fully understand the complexities of normal kidney function. There is also the opportunity to integrate data in three and four dimensions both in vitro and in vivo . Determining the most efficient way to leverage the growing amount of such complex “omics” data into a better understanding of kidney function and new therapeutic strategies represents an additional critical next step. It will require advances in analytical tools, such as predictive mathematical models, and increased access to large sets of data in a variety of formats.

Kidney Function Across the Lifespan

Understanding the structure and function of the kidney throughout its life history (from early development to aged adult) remains a neglected field of study. The basic science research community is poised to undertake these studies using an integrated approach that draws on genetics, physiology, and developmental, molecular, and cellular biology. Little is known about the changes in kidney in response to organismal life history, including the cellular and molecular basis involved in maintaining or resetting physiologic homeostasis to adjust BP between the juvenile and adult or respond to circulating hormones (puberty and menopause) or diet (weaning). The molecular basis for the increased susceptibility of the aged kidney to acute and chronic damage is also largely unknown. This area holds enormous and largely untapped potential to inform clinical considerations.

Loss of Homeostasis

We encourage traditional fields of normal kidney biology to consider the study of kidney disease as a loss of homeostasis. An unrecognized concept is the idea of homeostatic productive repair that maintains kidney and nephron health on a day-to-day basis in the absence of dramatic challenges. Indeed, the loss of homeostatic repair may be part of the etiology of increased kidney disease observed in the elderly. Current kidney injury models largely focus on the response to severe or catastrophic injury, such as those responses triggered by ischemia, sepsis, or nephrotoxins. However, debilitating kidney injury in humans is generally superimposed on an underlying chronic disorder and/or occurs in the elderly. This dichotomy emphasizes the need to understand the changes in the physiologic regulation and the homeostatic repair processes throughout the life history of the kidney, especially the aged kidney. It is relevant to one of the most common kidney diseases (diabetic nephropathy), which can take many years to develop in humans, and, perhaps, because of this fact, it has been very difficult to model in mice. If the effectiveness of targeted therapies proves to be too limited in the future, more comprehensive strategies should be considered ( i.e. , efforts involving system biology, integrative biology, and system medicine).

The study of kidney physiology, cell biology, and development has been, and remains, the foundation for understanding renal disease. Research in these areas provides opportunities to further characterize largely neglected cell types, define contributions of other physiologic systems tightly integrated with the functioning kidney, and incorporate normal variables, such as fetal nutrition, aging, and the life history of the kidney, into ongoing and future studies. Initial data may be available from Murine Atlas of Genitourinary Development, an NIDDK-supported consortium designed to define the molecular and cellular anatomy of the murine kidney through developmental time. Insights from such efforts provide essential baselines for understanding normal changes in renal structure/function, response to injury, and, ultimately, the broad spectrum of kidney diseases. The increased ability to develop targeted genetic and pharmacologic interventions to correct individual pathways and proteins defective in disease offers an extraordinary opportunity to treat or cure these disorders.

The six areas of investigation mentioned above suggest important crosscutting themes and opportunities for broadly informing kidney research. Basic physiologic and cell biologic studies of hormone receptors, signal transduction pathways, regulation by microRNA, and mechanisms (such as protein–protein interactions, protein phosphorylation, protein trafficking, and the role of degradation) will elucidate novel regulatory pathways and identify previously unrecognized therapeutic targets. Such crosscutting fundamental studies are especially important in designing therapies that may compensate for a mutant gene or predict an otherwise unexpected complication from a therapy aimed at a particular target. These studies may also contribute to novel strategies for maintenance of better kidney health over its life history.

Disclosures

B.D.H. is funded by a grant from Evotec with the goal of discovering new therapeutic targets to treat acute kidney disease and CKD. A.P.M. is in collaboration around kidney disease with Evotec, for which the laboratory of A.P.M. receives research support from Evotec.

Acknowledgments

The Kidney Research National Dialogue was developed and implemented by the National Institute of Diabetes and Digestive and Kidney Diseases/Division of Kidney, Urologic and Hematologic Diseases (KUH) staff and directed by Dr. Krystyna Rys-Sikora. The Normal Kidney Development, Cell Biology, and Physiology topic was facilitated by C.M. and D.H. Please visit the Kidney Research National Dialogue website http://www2.niddk.nih.gov/KUH/KUHHome/KRND.htm for full details or to post comments about this review.

Published online ahead of print. Publication date available at www.cjasn.org .

Review Questions

Diabetes insipidus or diabetes mellitus would most likely be indicated by ________.

• none of the above

The color of urine is determined mainly by ________.

• filtration rate
• byproducts of red blood cell breakdown
• filtration efficiency

Production of less than 50 mL/day of urine is called ________.

Peristaltic contractions occur in the ________.

• urethra, bladder, and ureters

Somatic motor neurons must be ________ to relax the external urethral sphincter to allow urination.

Which part of the urinary system is not completely retroperitoneal?

The renal pyramids are separated from each other by extensions of the renal cortex called ________.

• renal medulla
• minor calyces
• medullary cortices
• renal columns

The primary structure found within the medulla is the ________.

• loop of Henle
• portal system

The right kidney is slightly lower because ________.

• it is displaced by the liver
• it is displace by the heart
• it is slightly smaller
• it needs protection of the lower ribs

Blood filtrate is captured in the lumen of the ________.

• Bowman’s capsule
• renal papillae

What are the names of the capillaries following the efferent arteriole?

• arcuate and medullary
• interlobar and interlobular
• peritubular and vasa recta
• peritubular and medullary

The functional unit of the kidney is called ________.

• the renal hilus
• the renal corpuscle
• the nephron

________ pressure must be greater on the capillary side of the filtration membrane to achieve filtration.

• Hydrostatic

Production of urine to modify plasma makeup is the result of ________.

• filtration, absorption, and secretion

Systemic blood pressure must stay above 60 so that the proper amount of filtration occurs.

Aquaporin channels are only found in the collecting duct.

Most absorption and secretion occurs in this part of the nephron.

• proximal convoluted tubule
• descending loop of Henle
• ascending loop of Henle
• distal convoluted tubule
• collecting ducts

The fine tuning of water recovery or disposal occurs in ________.

• the proximal convoluted tubule
• the collecting ducts
• the ascending loop of Henle
• the distal convoluted tubule

Vasodilation of blood vessels to the kidneys is due to ________.

• more frequent action potentials
• less frequent action potentials

When blood pressure increases, blood vessels supplying the kidney will ________ to mount a steady rate of filtration.

Which of these three paracrine chemicals cause vasodilation?

• nitric oxide

What hormone directly opposes the actions of natriuretic hormones?

• aldosterone

Which of these is a vasoconstrictor?

• natriuretic hormone
• angiotensin II

What signal causes the heart to secrete atrial natriuretic hormone?

• increased blood pressure
• decreased blood pressure
• increased Na + levels
• decreased Na + levels

Which of these beverages does not have a diuretic effect?

Progesterone can bind to receptors for which hormone that, when released, activates water retention?

Renin is released in response to ________.

Which step in vitamin D production does the kidney perform?

• converts cholecalciferol into calcidiol
• converts calcidiol into calcitriol
• stores vitamin D
• none of these

Which hormone does the kidney produce that stimulates red blood cell production?

• thrombopoietin

If there were no aquaporin channels in the collecting duct, ________.

• you would develop systemic edema
• you would retain excess Na +
• you would lose vitamins and electrolytes
• you would suffer severe dehydration

As an Amazon Associate we earn from qualifying purchases.

This book may not be used in the training of large language models or otherwise be ingested into large language models or generative AI offerings without OpenStax's permission.

Want to cite, share, or modify this book? This book uses the Creative Commons Attribution License and you must attribute OpenStax.

Access for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction

• Authors: J. Gordon Betts, Kelly A. Young, James A. Wise, Eddie Johnson, Brandon Poe, Dean H. Kruse, Oksana Korol, Jody E. Johnson, Mark Womble, Peter DeSaix
• Publisher/website: OpenStax
• Book title: Anatomy and Physiology
• Publication date: Apr 25, 2013
• Location: Houston, Texas
• Book URL: https://openstax.org/books/anatomy-and-physiology/pages/1-introduction
• Section URL: https://openstax.org/books/anatomy-and-physiology/pages/25-review-questions

© Jan 27, 2022 OpenStax. Textbook content produced by OpenStax is licensed under a Creative Commons Attribution License . The OpenStax name, OpenStax logo, OpenStax book covers, OpenStax CNX name, and OpenStax CNX logo are not subject to the Creative Commons license and may not be reproduced without the prior and express written consent of Rice University.