Why is erythropoietin produced in the kidney?

Why is erythropoietin produced in the kidney?

We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Erythropoietin is a hormone produced in the kidney to stimulate the generation of more red blood cell. It is triggered by low oxygen via HIF transcription factors. Makes sense. Oops, oxygen is low, let's make more erythrocytes to carry more oxygen from the lung to consuming cells.

What doesn't make sense is why evolution would locate the production of EPO in the kidneys. These are organs tasked with excretion via the urine - pump and retrieve. They have very little to do with red blood cell gas exchange (lungs), generation (bone marrow), or removal (spleen).

Can somebody think of a good reason why you would locate the synthesis and release of the primary hormone to trigger red blood cell generation in a seemingly unrelated organ like the kidneys?

Medical Definition of Hormone, erythropoietin

Hormone, erythropoietin: Erythropoietin is a substance produced by the kidney that leads to the formation of red blood cells in the bone marrow. Abbreviated: EPO.

The kidney cells that make EPO are specialized and are sensitive to low oxygen levels in the blood coming into the kidney. These cells release erythropoietin when the oxygen level is low in the kidney. Erythropoietin stimulates the bone marrow to produce more red blood cells which in turn increases the oxygen-carrying capacity of the blood.

EPO is the prime regulator of red cell production. Its major functions are to promote the differentiation and development of red blood cells and to initiate the production of hemoglobin, the molecule within red cells that transports oxygen.

EPO is produced not only in the kidney but also, to a lesser extent, in the liver. The EPO gene has been found on human chromosome 7 (in band 7q21). Different DNA sequences flanking the EPO gene act to control liver versus kidney production of EPO.

The measurement of EPO in the blood can indicate bone marrow disorders or kidney disease. Normal levels of EPO are 0 to 19 mU/ml (milliunits per milliliter). Elevated levels can be seen in polycythemia rubra vera, a disorder characterized by an excess of red blood cells. Lower than normal values of EPO are seen in chronic renal failure.

Using recombinant DNA technology, EPO has been synthetically produced for use in persons with certain types of anemia: anemia due to kidney failure, anemia secondary to AZT treatment of AIDS , and anemia associated with cancer.

EPO has been much misused as a performance-enhancing drug in endurance athletes such as reportedly cyclists (in the Tour de France), long-distance runners, speed skaters, and Nordic (cross-country) skiers. When misused in such situations, EPO is thought to be especially dangerous (perhaps because dehydration can further increase the viscosity of the blood, increasing the risk for heart attacks and strokes. EPO has been banned by the Tour, the Olympics, and other sports organizations.



Erythropoietin is a glycoprotein hormone that is normally produced in the kidneys and is responsible for the stimulation of red blood cell production. The three synthetic preparations of erythropoietin available for clinical use are epoetin alfa, epoetin beta, and epoetin omega. Epoetin alfa and beta are both produced in CHO cells, whereas epoetin omega is produced in BHK cells. All are produced using recombinant DNA techniques and have an amino acid sequence that is identical to endogenous erythropoietin, but differ in the glycosylation pattern Product Information Procrit (2000) , Product Information Epogen (2000) Anon (1987) , Erslev (1987) . Recombinant epoetin has the same biological activity as the endogenous hormone, which induces erythropoiesis by stimulating the division and differentiation of committed erythroid progenitor cells Stockenhuber et al (1990) Product Information Epogen (2000) Schwenk and Halstenson (1989) . Erythropoietin also stimulates the release of reticulocytes into the blood stream from the bone marrow Schwenk and Halstenson (1989) . Epoetin alfa is used for the treatment of anemia and to reduce the need for blood transfusions in anemic patients undergoing surgery. The onset of activity is approximately 7–10 days, but can be up to six weeks Product Information Procrit (2000) , Product Information Epogen (2000) Eschbach et al (1987) , Zins et al (1986) , Winearls et al (1986) . During treatment, hematocrit, and platelet count should be monitored at regular intervals Product Information Procrit (2000) , Product Information Epogen (2000) .

In recent years, there has been an increase in the use of recombinant human erythropoietin (rhEPO) to enhance athletic performance by increasing oxygen transport to tissues. This procedure has been banned by many sports organizations. However, there are problems with directly testing for rhEPO in blood or urine because of its short half-life and it similar structure to endogenous erythropoietin.

Regulation of urine production

The permeability of the distal tubule and collecting duct is controlled by a hormone called anti-diuretic hormone (ADH).

ADH is secreted by a gland attached to the hypothalamus called the pituitary gland. Anti-diuretic hormone increases the permeability of the distal tubule and collecting duct, thus allowing more water to be removed from the nephric filtrate when the body has a need to conserve water.

The pituitary gland is controlled by the hypothalamus.

The hypothalamus acts to regulate the body’s feedback systems. When the body needs to eliminate excess water, anti-diuretic hormone is inhibited and more water is excreted in the urine. Drugs such as alcohol and caffeine block the release of ADH and increase the volume of urine.

Erythropoietin (EPO, The EPO Test)

Erythropoietin (EPO) is a hormone produced by the kidney that promotes the formation of red blood cells by the bone marrow.

The kidney cells that make erythropoietin are sensitive to low oxygen levels in the blood that travels through the kidney. These cells make and release erythropoietin when the oxygen level is too low. A low oxygen level may indicate a diminished number of red blood cells (anemia), or hemoglobin molecules that carry oxygen through the body.

What does erythropoietin do? Why do we need it?

Erythropoietin stimulates the bone marrow to produce more red blood cells. The resulting rise in red cells increases the oxygen-carrying capacity of the blood.

As the prime regulator of red cell production, erythropoietin's major functions are to:

  1. Promote the development of red blood cells.
  2. Initiate the synthesis of hemoglobin, the molecule within red blood cells that transports oxygen.

Chemically, erythropoietin a protein with an attached sugar (a glycoprotein). It is one of a number of similar glycoproteins that serve as stimulants for the growth of specific types of blood cells in the bone marrow.

Erythropeoietin (EPO) Blood Doping

Lance cheated. Deep in our hearts we knew it, but until the words came out of his mouth, there was a glimmer of hope that he still could be our hero. Now he has fallen, admitting that he blood doped, used steroids and erythropoietin (EPO), and exhibited disdain to those around him, both friend and foe. The problem, however, is that sports are always filled with cheating, and the public accepts some acts of dishonesty as part of the game. The distinction between what is ethically acceptable and what is not continues to be a blurred line.

Muscle cells are factories that take the raw materials, oxygen and glucose, and turn them into energy. Training increases the ability of the body to deliver oxygen to the cells and increases muscle size. More efficiency and more power yield better athletic performance. Increasing the number of red blood cells in the body increases the ability to deliver oxygen to tissues and that's where blood doping and EPO come in.

What organ produces erythropoietin?

Erythropoietin is produced to a lesser extent by the liver. Only about 10% of erythropoietin is produced in the liver. The erythropoietin gene has been found on human chromosome 7 (in band 7q21). Different DNA sequences flanking the erythropoietin gene act to control liver versus kidney production of erythropoietin.

Why is an erythropoietin test performed?

The erythropoietin hormone can be detected and measured in the blood. An abnormal level of erythropoietin in the blood can indicate bone marrow disorders, (such as polycythemia, or increased red blood cell production) kidney disease, or erythropoietin abuse. Testing erythropoietin blood levels is of value if:

  • Too little erythropoietin might be responsible for too few red blood cells (anemia), especially anemia related to kidney disease.
  • Too much erythropoietin might be causing too many red blood cells (polycythemia).
  • Too much erythropoietin might be evidence for a kidney tumor.
  • Too much erythropoietin in an athlete may suggest erythropoietin abuse.

Do I need to fast before an erythropoietin blood test?

The patient is usually asked to fast for 8-10 hours (overnight) and sometimes to lie quietly and relax for 20 or 30 minutes before the test. The test requires a routine sample of blood, which is sent to the laboratory for analysis.

What are normal erythropoietin levels?

Normal levels of erythropoietin range from 4 up to 24 mU/ml (milliunits per milliliter).


What does an abnormal erythropoietin level mean?

Abnormal erythropoietin levels suggest possible disease of the bone marrow or kidneys. Another possibility is abuse by an athlete to increase the red cell count for better athletic performance. The correct interpretation of an abnormal erythropoietin level depends on the particular clinical situation. Sometimes, the erythropoetin level may be inappropriately normal when it should be elevated (such as when there is an anemia), indicating a problem with the kidneys.

Can a person without a medical disease or condition have a high erythropoietin (EPO) level?

Yes. For example, erythropoietin has been misused as a performance-enhancing drug in athletes such as cyclists (in the Tour de France), long-distance runners, speed skaters, and Nordic (cross-country) skiers. When misused in such situations, erythropoietin is thought to be especially dangerous (perhaps because dehydration due to vigorous exercise can further increase the thickness (viscosity) of the blood, raising the risk for blood clots, heart attacks, and strokes. Erythropoietin has been banned by the Tour de France, the Olympics, and other sports organizations.

Is erythropoietin available as a prescribed medication?

Yes. Using recombinant DNA technology, erythropoietin has been synthetically produced for use as a treatment for persons with certain types of anemia. Erythropoietin can be used to correct anemia by stimulating red blood cell production in the bone marrow in these conditions. The medication is known as epoetin alfa (Epogen, Procrit) or as darbepoietin alfa (Arnesp). It can be given as an injection intravenously (into a vein) or subcutaneously (under the skin).

Eugene Goldwasser, biochemist behind blockbuster anemia drug, 1922–2010

Eugene Goldwasser, the scientist who first purified erythropoietin—the hormone that stimulates the production of red blood cells—died from complications related to advanced prostate cancer on Friday, Dec. 17 at his Hyde Park home. He was 88.

Generally regarded as the “father of EPO,” a drug that helped launch the biotechnology revolution, Goldwasser was the Alice Hogge and Arthur A. Baer Professor Emeritus of Biochemistry and Molecular Biology. He led the team that, after 25 years of concentrated effort, purified the sheep form of erythropoietin, then the human variety. The discovery has enabled millions of dialysis patients and anemic patients with other diseases to live longer and more productive lives.

“Gene Goldwasser was such a nice, quiet, unassuming guy, you would never know that he had done something so absolutely monumental,” said colleague Donald Steiner, the A.N. Pritzker Distinguished Service Professor of Biochemistry and Molecular Biology. “His work with erythropoietin has had enormous impact. It is one of the great contributions to science or medicine of the 20th century, comparable to the discovery of insulin.”

A prolific researcher and author, Goldwasser published more than 150 research studies and 60 book chapters—almost all of them about some aspect of erythropoietin, also known as “epo.” He authored two short books: a biography of his mentor, Leon Jacobson, and a recently completed history of the quest for erythropoietin, which should come out in 2011.

“He was someone who took enormous delight in doing science,” said Gary Toback, professor of medicine. “He was also a valued mentor, colleague and friend.”

Although unsuccessful in persuading UChicago to patent his discovery—a novel concept at the time—Goldwasser worked as a consultant for the start–up biotechnology company, Amgen, sharing his expertise, methods and some of his purified erythropoietin to help them discover and clone the erythropoietin gene. Amgen patented the production of recombinant erythropoietin in 1987 and secured FDA approval of the drug in 1989 for treatment of anemia in patients undergoing dialysis. Although patent squabbles persisted for two more decades, the market for erythropoietin quickly blossomed to several billion dollars a year.

“One percent of one percent of the drug’s annual revenues,” Goldwasser wistfully noted years later, “would have funded my lab quite handsomely.”

‘Thought it would be a short diversion’

It was a request from Jacobson, who ran the University’s Argonne Cancer Research Hospital after World War II, which triggered Goldwasser’s interest in this hormone, which he initially considered “just a laboratory curiosity.” Jacobson wanted to understand how the blood–forming process recovered after radiation exposure. So in 1955 he asked Goldwasser to isolate and purify the biochemical signal that regulated the growth of new red blood cells.

“I thought it would be a short diversion for about six months, and then I’d get back to other research,” Goldwasser recalled.

In 1957, by removing various organs from rats and looking for the onset of anemia, he had traced production of the signal to the kidneys, which explained why patients with chronic kidney disease were often anemic and suggested that erythropoietin could be found in urine.

By 1971 his lab had purified 6 millionths of an ounce of the hormone from 125 gallons of plasma from anemic sheep. Erythropoietin, he noted in a press statement at the time, “is present, even in enriched sources, in an extremely minute amount.”

The breakthrough came in 1973, when Takaji Miyake, a Japanese physician who cared for patients suffering from aplastic anemia, contacted Goldwasser. They agreed to collaborate. While Goldwasser procured funding, Miyake collected 2,550 liters of urine from his patients. On Christmas Day 1975, he arrived in Chicago with his concentrated samples. Within 18 months they had eight precious milligrams of the potent human hormone. “We put it in rats,” recalled Goldwasser, “and it worked like a charm.”

Epo goes from trial to industrial production

Most of the existing supply went to a small, unpublished clinical trial, development of an assay to measure hormone levels in the blood, and early attempts to determine the amino–acid composition, a first step toward cloning the gene. In 1977, at the urging of colleagues and the federal agencies that funded his lab—the Department of Energy and the National Institutes of Health—Goldwasser filled out the patent disclosure form and submitted it to the University.

“After submitting the form, I promptly forgot about it,” he wrote years later, “since nothing was ever done about filing for a patent. I believe the rules at the time would have allowed me to file a patent for myself if the agency or the University decided not to—another point to perhaps be rueful about.”

Filing for patents “was not generally done at the time,” noted Toback.

Fledgling biotech companies, however, recognized the potential of Goldwasser’s discoveries. Several, including Biogen and Applied Molecular Genetics (now Amgen) sought his guidance.

“Biogen asked Gene to join their board of epo advisors,” recalled Chicago colleague, Robert Haselkorn, professor of biochemistry and molecular genetics. “Gene looked at the list of others on the board and decided that they were mediocre. Then, Amgen went through the same exercise and asked Gene to be their sole advisor on epo. He accepted, declining the board role but signing on as a consultant.” In 1985, a team from Amgen cloned the gene using two probes derived from amino acid sequence analysis of Goldwasser’s purified human erythropoietin samples. “The rest is history.”

By 1986, industrial production was under way. The first reports from clinical studies appeared in late 1986 and 1987, confirming that the drug could correct anemia in patients with kidney failure. By 1996, annual sales in the United States exceeded $1 billion. Amgen subsequently funded a professorship in Goldwasser’s department.

“The enormous success of epo still astonishes me,” Goldwasser wrote in a 1996 biographical essay. “It is still gratifying to me to see how effective epo is in correcting the anemia of dialysis patients, and how it spares them repeated transfusions.”

Less gratifying was the subsequent recognition, in the late 1990s, that athletes had been injecting the drug to boost their red blood cell counts for a competitive advantage. In 1998, an epo–based doping scandal resulted in expulsion or withdrawal for one–third of the 21 teams in the Tour de France, a development that deeply dismayed Goldwasser.

The benefits of his discovery however, far outweighed its potential for abuse. “Recombinant human erythropoietin is arguably the most successful therapeutic application of recombinant DNA technology to date,” said a 2009 editorial in the New England Journal of Medicine. “Since the initial reports … documented a cure of the anemia of chronic kidney disease with recombinant human erythropoietin, well over a million patients have been treated with it effectively and with minimal drug–related toxicity.”

Esteemed career at UChicago

Born Oct. 14, 1922, Goldwasser spent his first decade in Brooklyn, N.Y, before the Depression forced his father to close his small clothing manufacturing business and move to Kansas City, where his brother ran a similar business. In high school, Goldwasser developed an interest in science. He won a scholarship to the University of Chicago, where he majored in biological sciences and, after the attack on Pearl Harbor, worked as a research assistant in the University’s Toxicity Laboratory, a federally funded program to assess chemical and biological risks. He completed his bachelor’s degree in biochemistry in March 1943.

He was drafted into the United States Army in 1944 and served for two years as a biochemist at Fort Detrick, Md., working on anthrax. In 1946, he returned to UChicago as a graduate student. He married Florence Cohen of Chicago in 1949 and completed his PhD in biochemistry in 1950. He spent the next two years in a post–doctoral fellowship studying nucleic acids (part of it alongside fellow post–doc James Watson, a future Nobel laureate) with Herman Kalckar at the Institute for Cytophysiology in Copenhagen, Denmark.

In 1952, Goldwasser returned to Chicago as an instructor in biochemistry. He stayed for the rest of his career, rising to professor of biochemistry and molecular biology in 1963 and chair of the department from 1984 to 1985. He retired at age 65 in 1987, but remained active in his laboratory and served again as department chair from 1994 to 1998. He also served as chair of the Committee on Developmental Biology from 1976 to 1991. Goldwasser retired again in 2002.

He received several honors, including election as a fellow of the American Academy of Arts & Sciences and, most recently, the 2005 Prince Mahidol Award, from Thailand, given for “outstanding performance and/or research in the field of medicine for the benefit of mankind.”

His first wife died in 1981. In 1986, he married Deone Jackman, a Hyde Park neighbor, who was introduced to him by a mutual friend. He is survived by Jackman three sons: Thomas, of San Francisco Matthew, of Chicago and James, of New York two step children, Tom and Tara Jackman and seven grandchildren.

His friends and children recall him as an avid and gifted photographer, sailor, traveler and, in his younger years, skier. “He loved art, music and the Blackhawks,” recalled James Goldwasser. He particularly liked reading, added Toback, “which may explain why two of his three sons are in the book business.”

A memorial service will be held at Rockefeller Memorial Chapel on Monday, Jan. 24 at 4 pm.

Chronic Renal Failure and Erythropoietin (EPO)

Erythropoietin (EPO) is a hormone mainly made by the kidneys and tells stem cells in the bone marrow to make more red blood cells. In chronic renal failure, less erythropoietin is produced so that patients are more likely to have fatigue and anemia. Therefore, knowing the link of chronic renal failure and erythropoietin is good for these patients.

How is kidney failure associated to erythropoietin?

In healthy kidneys, the kidney cells that make erythropoietin are specialized so that they are sensitive to low oxygen levels in the blood. When anemia, low red blood cell, and other complications due to low oxygen level occur, the healthy kidney cells can produce more EPO so that these complications can be remitted spontaneously. However, once the kidneys are damaged severely, they can&rsquot make enough EPO any more and then the above symptoms like anemia may occur easily.

EPO, in turn, can also worsen kidney failure patients&rsquo condition, because lack of red blood cells leads to less blood and oxygen transported into the kidneys and then more than more kidney cells lose their ability to work gradually.

How to deal with lack of erythropoietin in chronic renal failure?

A healthy diet rich in nutrition and iron and correct medicines can be helpful. For people with kidney failure and severe anemia, erythropoietin is usually given by subcutaneous injection initially three times a week in conjunction with an oral iron supplement. The does of medicines changes with patients&rsquo red blood cell count test. Generally, patients&rsquo erythropoietin problem can be controlled very well after the treatment.

However, even though these medicines can help ease anemia and fatigue as well as some other complications, patients&rsquo damaged kidneys can&rsquot get any improvement. To increase patients&rsquo overall health, repairing impaired kidney cells is a must. Two remedies can help achieve this goal: Micro-Chinese Medicine Osmotherapy and Immunotherapy. Both of them have their own application scope, so you should choose a better treatment according to your specific condition.

Once part of kidney function recovers to work again, it can produce enough EPO by itself so that you won&rsquot take any medicines to stimulate the formation of red blood cells. If any confusion, you can leave a message to us or consult online.

Leave Message

Leave your problem to us,You will surely get the free medical advice from experts within 24 hours!

Related articles


Erythropoietin is distinct among the hematopoietic growth factors because it is produced primarily in the kidneys rather than the bone marrow. The kidney functions as a critmeter in that it senses oxygen tension and extracellular volume. By regulating red cell mass through erythropoietin and plasma volume through excretion of salt and water, the kidney sets the hematocrit at a normal value of 45%. This is not a random number, but a value that maximizes oxygen delivery to peripheral tissues. The ability of the kidney to coordinate these two volumes to generate a hematocrit of 45% establishes it as the logical site for erythropoietin production. The kidney has the unique ability to translate a measure of plasma volume as tissue oxygen pressure required to regulate erythropoietin production. I hypothesize that the critmeter is a functional unit that regulates the hematocrit. The critmeter is found at the tip of the juxtamedullary region of the cortical labyrinth in the kidney, where erythropoietin is made physiologically. Renal vasculature and nephron segment heterogeneity in sodium reabsorption generate the marginal tissue oxygen pressure required to trigger the production of erythropoietin. The balance of the oxygen consumption for sodium reabsorption and the oxygen delivery to the proximal tubule is reflected by the tissue oxygen pressure that determines red blood cell mass adjusted to plasma volume. Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter (eg, angiotensin II). Examples of clinical disorders caused by dysfunction or resetting of the critmeter are described. [copy ] 2001 by the National Kidney Foundation, Inc.

Supported by the Kidney Foundation of Canada.


Our editors will review what you’ve submitted and determine whether to revise the article.

Erythropoietin, hormone produced largely in the kidneys that influences the rate of production of red blood cells (erythrocytes). When the number of circulating red cells decreases or when the oxygen transported by the blood diminishes, an unidentified sensor detects the change, and the production of erythropoietin is increased. This substance is then transported through the plasma to the bone marrow, where it accelerates the production of red cells.

The erythropoietin mechanism operates like a thermostat, increasing or decreasing the rate of red cell production in accordance with need. When a person who has lived at high altitude moves to a sea level environment, production of erythropoietin is suppressed, the rate of red cell production declines, and the red cell count falls until the normal sea level value is achieved. With the loss of one pint of blood, the erythropoietin mechanism is activated, red cell production is enhanced, and within a few weeks the number of circulating red cells has been restored to the normal value. The precision of control is extraordinary so that the number of new red cells produced accurately compensates for the number of cells lost or destroyed.

Erythropoietin has been produced in vitro (outside the body) using recombinant DNA technology. The purified recombinant hormone has promise for persons with chronic renal failure, who develop anemia because of a lack of erythropoietin. Erythropoietin was the first hematopoietic growth factor to be developed for therapeutic purposes. In addition to treating anemia associated with chronic renal failure, it is used to treat anemia associated with zidovudine (AZT) therapy in patients infected with HIV. It may also be useful in reversing anemia in cancer patients receiving chemotherapy. Erythropoietin also has been administered after strokes in an effort to induce or enhance the growth of neurons, thereby staving off brain damage and spurring functional recovery.

This article was most recently revised and updated by Kara Rogers, Senior Editor.

The Kidneys

The kidneys are a pair of bean-shaped organs just above the waist. They are important organs with many functions in the body, including producing hormones, absorbing minerals, and filtering blood and producing urine.

A cross-section of a kidney is shown in Figure below. The function of the kidney is to filter blood and form urine. Urine is the liquid waste product of the body that is excreted by the urinary system. Wastes in the blood come from the normal breakdown of tissues, such as muscles, and from food. The body uses food for energy. After the body has taken the nutrients it needs from food, some of the wastes are absorbed into the blood. If the kidneys did not remove them, these wastes would build up in the blood and damage the body.

Kidneys and Nephrons

The actual removal of wastes from the blood occurs in tiny units inside the kidneys called nephrons. Nephrons are the structural and functional units of the kidneys. A single kidney may have more than a million nephrons! This is further discussed in the Urinary Systemconcept.

Each kidney is supplied by a renal artery and renal vein.

Kidneys and Homeostasis

The kidneys play many vital roles in homeostasis. They work with many other organ systems to do this. For example, they work with the circulatory system to filter blood, and with the urinary system to remove wastes.

The kidneys filter all the blood in the body many times each day and produce a total of about 1.5 liters of urine. The kidneys control the amount of water, ions, and other substances in the blood by excreting more or less of them in urine. The kidneys also secrete hormones that help maintain homeostasis. Erythropoietin, for example, is a kidney hormone that stimulates bone marrow to produce red blood cells when more are needed. They also secrete renin, which regulates blood pressure, and calcitriol, the active form of vitamin D, which helps maintain calcium for bones. The kidneys themselves are also regulated by hormones. For example, antidiuretic hormone from the hypothalamus stimulates the kidneys to produce more concentrated urine when the body is low on water.

Other Functions

In addition to filtering blood and producing urine, the kidneys are also involved in maintaining the water level in the body, and regulating red blood cell levels and blood pressure.

  • As the kidneys are mainly involved in the production of urine, they react to changes in the body&rsquos water level throughout the day. As water intake decreases, the kidneys adjust accordingly and leave water in the body instead of helping remove it through the urine, maintaining the water level in the body.
  • The kidneys also need constant pressure to filter the blood. When the blood pressure drops too low, the kidneys increase the pressure. One way is by producing angiotensin, a blood vessel-constricting protein. This protein also signals the body to retain sodium and water. Together, the constriction of blood vessels and retention of sodium and water help restore normal blood pressure.
  • When the kidneys don&rsquot get enough oxygen, they send out a signal in the form of the hormone erythropoietin, which stimulates the bone marrow to produce more oxygen-carrying red blood cells.