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15.6.1.6: Adrenal Glands - Biology

15.6.1.6: Adrenal Glands - Biology


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The adrenal glands are two small structures situated one atop each kidney. Both in anatomy and in function, they consist of two distinct regions an outer layer, the drenal ortex, which surrounds the adrenal medulla.

The Adrenal Cortex

Using cholesterol as the starting material, the cells of the adrenal cortex secrete a variety of steroid hormones. These fall into three classes:

  • glucocorticoids (e.g., cortisol)
  • mineralocorticoids (e.g., aldosterone)
  • androgens (e.g., testosterone)

Production of all three classes is triggered by the secretion of ACTH from the anterior lobe of the pituitary.

These hormones achieve their effects by:

  • Travelling through the body in the blood. Because they are so hydrophobic, they must be carried bound to a serum globulin.
  • Entering from the blood into all cells.
  • Binding to their recepto - a protein present in the cytoplasm and/or nucleus of "target" cells.
  • The hormone-receptor complex binds to a second to form a homodimer.
  • The homodimer migrates into the nucleus (if it did not form there) where it binds to specific hormone response elements in DNA.
  • These are specific DNA sequences in the promoter of genes that will be turned on (or off) by the interaction.
  • Other transcription factors are recruited to the promoter and gene transcription begins at some genes and is inhibited at others.

Glucocorticoids

The glucocorticoids get their name from their effect of raising the level of blood sugar (glucose). One way they do this is by stimulating gluconeogenesis in the liver: the conversion of fat and protein into intermediate metabolites that are ultimately converted into glucose.

The most abundant glucocorticoid is cortisol (also called hydrocortisone). Cortisol and the other glucocorticoids also have a potent anti-inflammatory effect on the body. They depress the immune response, especially cell-mediated immune responses.

For this reason glucocorticoids are widely used in therapy:

  • to reduce the inflammatory destruction of rheumatoid arthritis and other autoimmune diseases
  • to prevent the rejection of transplanted organs
  • to control asthma

Mineralocorticoids

The mineralocorticoids get their name from their effect on mineral metabolism. The most important of them is the steroid aldosterone. Aldosterone acts on the kidney promoting the reabsorption of sodium ions (Na+) into the blood. Water follows the salt and this helps maintain normal blood pressure.

Aldosterone also

  • acts on sweat glands to reduce the loss of sodium in perspiration
  • acts on taste cells to increase the sensitivity of the taste buds to sources of sodium.

The secretion of aldosterone is stimulated by:

  • a drop in the level of sodium ions in the blood
  • a rise in the level of potassium ions in the blood
  • angiotensin II
  • ACTH (as is that of cortisol)

Androgens

The adrenal cortex secretes precursors to androgens such as testosterone.

In sexually-mature males, this source is so much lower than that of the testes that it is probably of little physiological significance. However, excessive production of adrenal androgens can cause premature puberty in young boys.

In females, the adrenal cortex is a major source of androgens. Their hypersecretion may produce a masculine pattern of body hair and cessation of menstruation.

Addison's Disease: Hyposecretion of the adrenal cortices

Addison's disease has many causes, such as

  • destruction of the adrenal glands by infection
  • their destruction by an autoimmune attack
  • an inherited mutation in the ACTH receptor on adrenal cells

The essential role of the adrenal hormones means that a deficiency can be life-threatening. Fortunately, replacement therapy with glucocorticoids and mineralocorticoids can permit a normal life.

Cushing's Syndrome: Excessive levels of glucocorticoids

In Cushing's syndrome, the level of glucocorticoids, especially cortisol, is too high.

It can be caused by:

  • excessive production of ACTH by the anterior lobe of the pituitary
  • excessive production by the adrenals themselves (e.g., because of a tumor), or (quite commonly)
  • as a result of glucocorticoid therapy for some other disorder such as rheumatoid arthritis or preventing the rejection of an organ transplant

The Adrenal Medulla

The adrenal medulla consists of masses of neurons that are part of the sympathetic branch of the autonomic nervous system. Instead of releasing their neurotransmitters at a synapse, these neurons release them into the blood. Thus, although part of the nervous system, the adrenal medulla functions as an endocrine gland.

The adrenal medulla releases adrenaline (also called epinephrine) and noradrenaline (also called norepinephrine). Both are derived from the amino acid tyrosine. Release of adrenaline and noradrenaline is triggered by nervous stimulation in response to physical or mental stress. The hormones bind to adrenergic receptors — transmembrane proteins in the plasma membrane of many cell types.

Some of the effects are:

  • increase in the rate and strength of the heartbeat resulting in increased blood pressure
  • blood shunted from the skin and viscera to the skeletal muscles, coronary arteries, liver, and brain
  • rise in blood sugar
  • increased metabolic rate
  • bronchi dilate
  • pupils dilate
  • hair stands on end ("gooseflesh" in humans)
  • clotting time of the blood is reduced
  • increased ACTH secretion from the anterior lobe of the pituitary

All of these effects prepare the body to take immediate and vigorous action.


Eighteen-year-old Gabrielle checks her calendar. It has been 42 days since her last menstrual period, which is two weeks longer than the length of the average woman’s menstrual cycle. Although many women would suspect pregnancy if their period was late, Gabrielle has not been sexually active. She is not even sure she is “late,” because her period has never been regular. Ever since her first period when she was 13 years old, her cycle lengths have varied greatly, and there are months where she does not get a period at all. Her mother told her that a girl’s period is often irregular when it first starts, but five years later, Gabrielle’s still has not become regular. She decides to go to the student health center on her college campus to get it checked out.

The doctor asks her about the timing of her menstrual periods and performs a pelvic exam. She also notices that Gabrielle is overweight, has acne, and excess facial hair. As she explains to Gabrielle, while these physical characteristics can be perfectly normal, in combination with an irregular period, they can be signs of a disorder of the endocrine — or hormonal — system called polycystic ovary syndrome (PCOS).

In order to check for PCOS, the doctor refers Gabrielle for a pelvic ultrasound and sends her to the lab to get blood work done. When her lab results come back, Gabrielle learns that her levels of androgens (a group of hormones) are high, and so is her blood glucose (sugar). The ultrasound showed that she has multiple fluid-filled sacs (known as cysts) in her ovaries. Based on Gabrielle’s symptoms and test results, the doctor tells her that she does indeed have PCOS.

PCOS is common in young women. It is estimated that 6-10% women of childbearing age have PCOS — as many as 1.4 million women in in Canada. You may know someone with PCOS, or you may have it yourself.

Read the rest of this chapter to learn about the glands and hormones of the endocrine system, their functions, how they are regulated, and the disorders ­­— such as PCOS ­­— that can arise when hormones are not regulated properly. At the end of the chapter, you will learn more about PCOS, its possible long-term consequences (including fertility problems and diabetes), and how these negative outcomes can sometimes be prevented with lifestyle changes and medications.


Steroid Hormones

A steroid hormone (such as estrogen) is made of lipids . It is fat soluble, so it can diffuse across a target cell’s plasma membrane , which is also made of lipids. Once inside the cell, a steroid hormone binds with receptor proteins in the cytoplasm . As you can see in Figure 9.3.2, the steroid hormone and its receptor form a complex — called a steroid complex — which moves into the nucleus , where it influences the expression of genes. Examples of steroid hormones include cortisol , which is secreted by the adrenal glands , and sex hormones, which are secreted by the gonads .

Figure 9.3.2 A steroid hormone crosses the plasma membrane of a target cell, binds with a receptor protein within the cytoplasm, and forms a complex that moves to the nucleus, where it affects gene expression.


Adrenal Nodules

Adrenal nodules are growths on the adrenal glands. You have 2 adrenal glands, one located above each kidney. The adrenal glands make several hormones that regulate your body’s:

Some adrenal nodules produce hormones that can cause serious medical problems. These are called functioning nodules. Nodules larger than 4 centimeters tend to be of more concern and may require surgery.

Types

There are 4 main types of adrenal nodules.

Nonfunctional adrenal adenoma. This is the most common type. It’s benign (not cancerous) and often causes no symptoms. Typically, these don’t require treatment.

Functioning adrenal adenoma. These make hormones that can cause problems and usually need to be removed.

Pheochromocytoma. These types of nodules are rare and usually benign. However, they can release hormones that cause:

Adrenal carcinoma. This is a very rare type of cancer that forms in the adrenal gland. These nodules can be functioning or nonfunctioning.

Symptoms

An adrenal nodule that’s not producing hormones generally doesn’t have symptoms. A functioning adrenal nodule may have different symptoms. This depends on which hormones are produced. Symptoms may include:

  • Changes in face and body shape
  • Acne
  • Unexplained weight gain or loss
  • High blood pressure
  • Muscle weakness
  • Diabetes
  • Increase in body hair in women
  • Occasional headaches and/or abdominal pain
  • Excessive sweating
  • Abnormal fatigue
  • Sexual dysfunction

Diagnosis

We order blood and urine tests to find out if the adrenal gland is making the right amounts of hormones. CT scans are also usually required to monitor the size of adrenal nodules.

Treatment

Most adrenal nodules don’t require treatment. We’ll monitor them to make sure they don’t change.

We may recommend treatment if a nodule is large (over 4 centimeters) and:

Some nodules may need to be surgically removed. If an adrenal nodule is causing high blood pressure, we may prescribe medications to control your blood pressure until surgery is performed.

Surgery

We use several techniques to remove adrenal nodules. The most effective approach will depend on your overall health and the size of the tumor.

Laparoscopic adrenalectomy. This is a minimally invasive procedure. It’s the most common surgery used to remove an adrenal nodule. During this procedure, the surgeon:

  • Makes small incisions in your abdomen.
  • Inserts long, thin instruments through the incisions. These instruments carry tiny fiber-optic cameras. They help the surgeon to guide the instruments to the adrenal gland.
  • Removes the gland containing the nodule through the incisions.

Hand-assisted laparoscopic surgery (HALS). This is very similar to a laparoscopic adrenalectomy. Special devices are used to remove larger tumors through a 2-inch incision.

Open surgery. This is done to remove very large nodules that are 5 to 6 centimeters or larger. The surgeon makes a larger incision through the abdomen or back.

If an adrenal nodule is cancerous, additional treatment may be necessary. Treatment may include chemotherapy, radiation therapy, and medication.

Living With Your Condition

After the removal of an adrenal nodule, you may require periodic follow-up examinations. You may need:

Steroids replace the hormones from the removed gland. Usually, the remaining adrenal gland will eventually produce enough of these hormones. If both glands were removed, you’ll need to take hormone replacement medications for the rest of your life, and you should wear a Medic Alert bracelet at all times.

You’ll also need to maintain a healthy diet and weight, and avoid smoking. A moderate exercise routine will help you regain energy and strength.

If you have an emergency medical condition, call 911 or go to the nearest hospital. An emergency medical condition is any of the following:
(1) a medical condition that manifests itself by acute symptoms of sufficient severity (including severe pain) such that you could reasonably expect the absence of immediate medical attention to result in serious jeopardy to your health or body functions or organs (2) active labor when there isn't enough time for safe transfer to a Plan hospital (or designated hospital) before delivery, or if transfer poses a threat to your (or your unborn child's) health and safety, or (3) a mental disorder that manifests itself by acute symptoms of sufficient severity such that either you are an immediate danger to yourself or others, or you are not immediately able to provide for, or use, food, shelter, or clothing, due to the mental disorder.

This information is not intended to diagnose health problems or to take the place of specific medical advice or care you receive from your physician or other health care professional. If you have persistent health problems, or if you have additional questions, please consult with your doctor. If you have questions or need more information about your medication, please speak to your pharmacist. Kaiser Permanente does not endorse the medications or products mentioned. Any trade names listed are for easy identification only.


Control of the Digestive Process

The process of digestion is controlled by both hormones and nerves. Hormonal control is mainly by endocrine hormones secreted by cells in the lining of the stomach and small intestine. These hormones stimulate the production of digestive enzymes, bicarbonate, and bile. The hormone secretin, for example, is produced by endocrine cells lining the duodenum of the small intestine. Acidic chyme entering the duodenum from the stomach triggers the release of secretin into the bloodstream. When the secretin returns via the circulation to the digestive system, it signals the release of bicarbonate from the pancreas. The bicarbonate neutralizes the acidic chyme. See Table 15.3.2 for a summary of the major hormones governing the process of chemical digestion.

Nerves involved in digestion include those that connect digestive organs to the central nervous system , as well as nerves inside the walls of the digestive organs. Nerves connecting the digestive organs to the central nervous system cause smooth muscles in the walls of digestive organs to contract or relax as needed, depending on whether or not there is food to be digested. Nerves within digestive organs are stimulated when food enters the organs and stretches their walls. These nerves trigger the release of substances that speed up or slow down the movement of food through the GI tract and the secretion of digestive enzymes.


4. Prostate Gland

In the normal prostatic epithelium, angiotensins stimulate cells proliferation. The addition of ACE inhibitor, captopril, resulted in a decreased incorporation of bromodeoxyuridine into cell nuclei (index of cell proliferation) of prostatic epithelial cells. Treatment with Ang II or Ang IV reversed the inhibition of proliferation induced by captopril. Moreover, this effect was not directed by AT1R, because addition of losartan did not block activity of angiotensin [75]. Angiotensins influence as well prostate cancer cells growth. Lawnicka et al. noticed that, in contrast to the normal prostatic epithelium, in the hormone-independent prostate cancer cell line, DU-145, angiotensin (Ang II, Ang III, Ang IV) caused concentration-dependent decrease of cell viability [55,76]. In contrary to this study, Domińska et al. observed that Ang II stimulates proliferation of the LNCaP (hormone-dependent prostate cancer) cell line, but not of the DU-145 cell line. Moreover, 24 h-incubation with Ang II resulted in inhibited cell growth. In both cell lines, treatment with Ang III caused weak increase of cell proliferation in DU-145 and LNCaP cell lines [19]. Sidorkiewicz et al. noticed that Ang II inhibited cells proliferation of the aforementioned cell line acting via AT1R. What is more, they discovered that there were two variants of AT1R in this cell line [77]. The other peptide from Ang family, Ang IV, also had effect on prostate cancer cells growth. Concerning the hormone-independent cell line, there was no significant influence of Ang IV on cell viability and proliferation, while in the case of the hormone-dependent cell line, Ang IV decreased cell growth. Moreover, the AT2R blocker (PD123319) reduced the inhibitory effect of Ang IV on proliferation of LNCaP cells, which implied that the proliferative activity of Ang IV could be mediated by AT2R. Interestingly, Ang IV was able to modulate AT1R and AT2R density in prostate cancer cells [78]. Domińska et al. reported that RAS and the relaxin family peptide system were correlated and had impact on the viability and proliferation of prostate cancer cells [79] and normal prostate epithelial cells [80]. In two prostate cancer cell lines, LNCaP (high androgen receptor activity, low invasiveness) and PC3 (low androgen receptor activity, highly metastatic), both peptides, Ang II and relaxin 2, induced proliferation, however, greater changes were observed in androgen-dependent cell line. Domińska et al. also observed a significant increase in androgen receptor expression in LNCaP cells but an insignificant decrease in PC3 [79]. In addition, treatment with peptides in combination had bigger impact than application of them separately [58]. Concerning the normal prostate epithelial cell line, PNT1A, there was similar effect of Ang II and RLN2 as in prostate cancer cell lines. Both peptides administered alone increased viability of PNT1A cells, but in combination, this effect was greater. Relating to the BrdU incorporation assay, both peptides increased proliferation, however this effect was very weak [81]. Ang II and RLN influenced proliferation and invasion of prostate epithelial and cancer cells by modulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) pathways [80]. Uemura et al. confirmed that Ang II stimulated proliferation of normal and cancer prostate cell, additionally this effect was inhibited by AT2R blockers [82].

As mentioned above, Ang II can influence cell proliferation, through modulation of TKs activity. Ang IV was capable of reducing TK activity and cell viability of the hormone-dependent prostate cancer cell line, LNCaP. Ang IV acted, at least partially, through AT2R, because addition of its blocker, PD123319, decreased inhibitory effect [83]. Domińska et al. observed that steroid hormones, testosterone, and 17β-estradiol were capable of reversion of the action of Ang II and Ang 1-7, which decreased protein TK activity in the late-stage prostate cancer cell line𠅍U145 [84]. Ito et al. noticed that inhibition of AT2R by its agonist, Compound 21 (C21), resulted in reduction of proliferation of prostate cancer cells and transgenic rat for adenocarcinoma of prostate (TRAP). Moreover, C21 decreased expression of androgen receptor and activity of prostate-specific antigen (PSA) promoter [85]. Woo et al. reported that AT2R blockers inhibited proliferation of prostate cancer cells. Moreover, in this study was observed that those blockers induced autophagy-associated cells death [86].

In prostate gland AT1R and AT2R, stromal and epithelial structures were found. Similarly, to endometrial cancer, the highest expression of these receptors was correlated with Gleason 2 grade (well differentiated) in neoplastic epithelium in comparison to non-neoplastic epithelium and Gleason 3-5 grade [49]. Moreover, the expression level of AT1R and AT2Rs in the rat prostate on protein and mRNA level was correlated with myocardial infarction [87]. Ang II and relaxin 2 can modulate expression of androgen receptors (ARs) in prostate cancer cells.


7.7 Review Questions

  1. What is the autonomic nervous system?
  2. How do the autonomic nervous system and endocrine system communicate with other organ systems so the systems can interact?
  3. Explain how the brain communicates with the endocrine system.
  4. What is the role of the pituitary gland in the endocrine system?
  5. Identify the organ systems that play a role in cellular respiration.
  6. How does the hormone adrenaline prepare the body to fight or flee? What specific physiological changes does it bring about?
  7. Explain the role of the muscular system in digesting food.
  8. Describe how three different organ systems are involved when a player makes a particular play in baseball, such as catching a fly ball.

About the Author

Gerard Tortora is Professor of Biology at Bergen Community College in Paramus, New Jersey, where he teaches human anatomy and physiology as well as microbiology. He received his bachelor&rsquos degree in biology from Fairleigh Dickinson University and his master's degree in science education from Montclair State College. He has been a member of many professional organizations, including the Human Anatomy and Physiology Society (HAPS). Gerard is the author of several best-selling science textbooks and laboratory manuals, a calling that often requires many additional hours per week beyond his teaching responsibilities. Nevertheless, he still makes time for four or five weekly aerobic workouts that include biking and running. He also enjoys attending college basketball and professional hockey games and performances at the Metropolitan Opera House.

Mark Nielsen is a Professor in the Department of Biology at the University of Utah. For the past 31 years he has taught anatomy, neuroanatomy, embryology, human dissection, comparative anatomy, and an anatomy teaching course to over 25,000 students. He has prepared and participated in hundreds of dissections of both humans and other vertebrate animals. All his courses incorporate a cadaver-based component to the training with an outstanding exposure to cadaver anatomy. He is a member of the American Association of Anatomists (AAA), the Human Anatomy and Physiology Society (HAPS), and the American Association of Clinical Anatomists (AACA).
Mark has a passion for teaching anatomy and sharing his knowledge with his students. In addition to the many students to whom he has taught anatomy, he has trained and served as a mentor for over 1,200 students who have worked in his anatomy laboratory as teaching assistants. His concern for students and his teaching excellence have been acknowledged through numerous awards.


Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats

Rats were maintained for 2 years on diets supplying 0.1, 0.01, and 0.001 μg of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg/day. Analysis of these diets indicated 2200, 210, and 22 parts per trillion (ppt) of TCDD. Ingestion of 0.1 μg/kg/day caused an increased incidence of hepatocellular carcinomas and squamous cell carcinomas of the lung, hard palate/nasal turbinates, or tongue, whereas a reduced incidence of tumors of the pituitary, uterus, mammary glands, pancreas, and adrenal gland was noted. Other indications of toxicity at this dose level included increased mortality, decreased weight gain, slight depression of erythroid parameters, increased urinary excretion of porphyrins and δ-aminolevulinic acid, along with increased serum activities of alkaline phosphatase, γ-glutamyl transferase and glutamic-pyruvic transaminase. Gross and histopathologic changes were noted in the hepatic, lymphoid, respiratory, and vascular tissues. The primary hepatic ultrastructural change at this high dose level was proliferation of the rough endoplasmic reticulum. Terminal liver and fat samples from rats at this high dose level contained 24,000 and 8100 ppt of TCDD, respectively. Rats given 0.01 μg/kg/day for 2 years had a lesser degree of toxicity than that seen at the highest dose level. This included increased urinary excretion of porphyrins in females, liver lesions (including hepatocellular nodules), and lung lesions (including focal alveolar hyperplasia). Terminal liver and fat samples from rats of this dose level contained 5100 and 1700 ppt of TCDD, respectively. Ingestion of 0.001 μg of TCDD/kg/day (∼22 ppt in the diet) caused no effects considered to be of any toxicologic significance. At this lower dose level, terminal liver and fat samples each contained 540 ppt of TCDD. These data indicate that continuous doses of TCDD sufficient to induce severe toxicity increased the incidence of some types of tumors, while reducing other types. During the 2-year study in rats, no increase in tumors occurred in those rats receiving sufficient TCDD to induce slight or no manifestations of toxicity.


Human Genetic Variation and Disease

An important benefit of studying human genetic variation is that we can learn more about the genetic basis of human diseases. The more we understand the causes of diseases, the more likely it is that we will be able to find effective treatments and cures for them.

Some disorders are caused by mutations in a single gene. Most of these disorders are generally rare, but some of them occur at significantly higher frequencies in certain populations. For example, Ellis-van Creveld syndrome has an unusually high frequency in Pennsylvania Amish populations, and Tay-Sachs disease has a relatively high frequency in Ashkenazi Jewish populations. Albinism is another single-gene disorder that has a variable frequency. In North America and Europe, rates of albinism are approximately 1:18,000. In Africa, in contrast, the rates range from 1:5,000 to 1:15,000. Some African populations have estimated albinism rates as high as 1:1000. The photo below (Figure 6.2.3) shows an African albino man from Mali, where there is a relatively high rate of albinism. High population-specific frequencies of single-gene disorders like these may be attributable to a variety of factors, such as small founding populations and a relative lack of gene flow.

Figure 6.2.3 This man from Mali exhibits the lack of pigmentation that is a hallmark of albinism.

It is likely that the majority of human diseases are caused by a complex mix of multiple genes (polygenic) and environmental factors (multifactorial). Examples of polygenic, multifactorial diseases are type II diabetes and heart disease . We do not typically think of these diseases as genetic diseases, because our genes do not predetermine whether we develop them. Our genes, however, do influence our chances of developing the diseases under certain environmental conditions. Even our chances of developing some infectious diseases are influenced by our genes. For example, a variant allele for a gene called CCR5 seems to confer resistance to infection with HIV , the virus that causes AIDS.


Watch the video: Οξέα και βάσεις κατά Arrhenius (July 2022).


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