37.6: Regulation of Body Processes - Hormonal Regulation of the Excretory System
- Page ID
- 13975
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\(\newcommand{\avec}{\mathbf a}\) \(\newcommand{\bvec}{\mathbf b}\) \(\newcommand{\cvec}{\mathbf c}\) \(\newcommand{\dvec}{\mathbf d}\) \(\newcommand{\dtil}{\widetilde{\mathbf d}}\) \(\newcommand{\evec}{\mathbf e}\) \(\newcommand{\fvec}{\mathbf f}\) \(\newcommand{\nvec}{\mathbf n}\) \(\newcommand{\pvec}{\mathbf p}\) \(\newcommand{\qvec}{\mathbf q}\) \(\newcommand{\svec}{\mathbf s}\) \(\newcommand{\tvec}{\mathbf t}\) \(\newcommand{\uvec}{\mathbf u}\) \(\newcommand{\vvec}{\mathbf v}\) \(\newcommand{\wvec}{\mathbf w}\) \(\newcommand{\xvec}{\mathbf x}\) \(\newcommand{\yvec}{\mathbf y}\) \(\newcommand{\zvec}{\mathbf z}\) \(\newcommand{\rvec}{\mathbf r}\) \(\newcommand{\mvec}{\mathbf m}\) \(\newcommand{\zerovec}{\mathbf 0}\) \(\newcommand{\onevec}{\mathbf 1}\) \(\newcommand{\real}{\mathbb R}\) \(\newcommand{\twovec}[2]{\left[\begin{array}{r}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\ctwovec}[2]{\left[\begin{array}{c}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\threevec}[3]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\cthreevec}[3]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\fourvec}[4]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\cfourvec}[4]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\fivevec}[5]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\cfivevec}[5]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\mattwo}[4]{\left[\begin{array}{rr}#1 \amp #2 \\ #3 \amp #4 \\ \end{array}\right]}\) \(\newcommand{\laspan}[1]{\text{Span}\{#1\}}\) \(\newcommand{\bcal}{\cal B}\) \(\newcommand{\ccal}{\cal C}\) \(\newcommand{\scal}{\cal S}\) \(\newcommand{\wcal}{\cal W}\) \(\newcommand{\ecal}{\cal E}\) \(\newcommand{\coords}[2]{\left\{#1\right\}_{#2}}\) \(\newcommand{\gray}[1]{\color{gray}{#1}}\) \(\newcommand{\lgray}[1]{\color{lightgray}{#1}}\) \(\newcommand{\rank}{\operatorname{rank}}\) \(\newcommand{\row}{\text{Row}}\) \(\newcommand{\col}{\text{Col}}\) \(\renewcommand{\row}{\text{Row}}\) \(\newcommand{\nul}{\text{Nul}}\) \(\newcommand{\var}{\text{Var}}\) \(\newcommand{\corr}{\text{corr}}\) \(\newcommand{\len}[1]{\left|#1\right|}\) \(\newcommand{\bbar}{\overline{\bvec}}\) \(\newcommand{\bhat}{\widehat{\bvec}}\) \(\newcommand{\bperp}{\bvec^\perp}\) \(\newcommand{\xhat}{\widehat{\xvec}}\) \(\newcommand{\vhat}{\widehat{\vvec}}\) \(\newcommand{\uhat}{\widehat{\uvec}}\) \(\newcommand{\what}{\widehat{\wvec}}\) \(\newcommand{\Sighat}{\widehat{\Sigma}}\) \(\newcommand{\lt}{<}\) \(\newcommand{\gt}{>}\) \(\newcommand{\amp}{&}\) \(\definecolor{fillinmathshade}{gray}{0.9}\)- Explain how the actions of different hormones regulate the excretory system
Hormonal Regulation of the Excretory System
Maintaining a proper water balance in the body is important to avoid dehydration or over-hydration (hyponatremia). The water concentration of the body is monitored by osmoreceptors in the hypothalamus, which detect the concentration of electrolytes in the extracellular fluid. The concentration of electrolytes in the blood rises when there is water loss caused by excessive perspiration, inadequate water intake, or low blood volume due to blood loss. An increase in blood electrolyte levels results in a neuronal signal being sent from the osmoreceptors in hypothalamic nuclei. The anterior pituitary is composed of glandular cells that secrete protein hormones. The pituitary gland has two components: anterior and posterior. The posterior pituitary is an extension of the hypothalamus. It is composed largely of neurons that are continuous with the hypothalamus.
Antidiuretic Hormone (ADH)
The hypothalamus produces a polypeptide hormone known as antidiuretic hormone (ADH), which is transported to and released from the posterior pituitary gland. The principal action of ADH is to regulate the amount of water excreted by the kidneys. As ADH (which is also known as vasopressin) causes direct water reabsorption from the kidney tubules, salts and wastes are concentrated in what will eventually be excreted as urine. The hypothalamus controls the mechanisms of ADH secretion, either by regulating blood volume or the concentration of water in the blood. Dehydration or physiological stress can cause an increase of osmolarity above threshold levels, which, in turn, raises ADH secretion and water retention, causing an increase in blood pressure. ADH travels in the bloodstream to the kidneys where it changes the kidneys to become more permeable to water by temporarily inserting water channels, aquaporins, into the kidney tubules. Water moves out of the kidney tubules through the aquaporins, reducing urine volume. The water is reabsorbed into the capillaries, lowering blood osmolarity back toward normal. As blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus; ADH secretion is reduced. ADH release can be reduced by certain substances, including alcohol, which can cause increased urine production and dehydration.
Chronic underproduction of ADH or a mutation in the ADH receptor results in diabetes insipidus. If the posterior pituitary does not release enough ADH, water cannot be retained by the kidneys and is lost as urine. This causes increased thirst, but water taken in is lost again and must be continually consumed. If the condition is not severe, dehydration may not occur, but severe cases can lead to electrolyte imbalances due to dehydration.
Another hormone responsible for maintaining electrolyte concentrations in extracellular fluids is aldosterone, a steroid hormone that is produced by the adrenal cortex. In contrast to ADH, which promotes the reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by enhancing Na+ reabsorption and K+ secretion from extracellular fluid of the cells in kidney tubules. Because it is produced in the cortex of the adrenal gland and affects the concentrations of minerals Na+ and K+, aldosterone is referred to as a mineralocorticoid, a corticosteroid that affects ion and water balance. Aldosterone release is stimulated by a decrease in blood sodium levels, blood volume, or blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na+ from sweat, saliva, and gastric juice. The reabsorption of Na+ also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.
Aldosterone production can be stimulated by low blood pressure, which triggers a sequence of chemical release. When blood pressure drops, the renin-angiotensin-aldosterone system (RAAS) is activated. Cells in the juxtaglomerular apparatus, which regulates the functions of the nephrons of the kidney, detect this and release renin. Renin, an enzyme, circulates in the blood, reacting with a plasma protein produced by the liver called angiotensinogen. When angiotensinogen is cleaved by renin, it produces angiotensin I, which is then converted into angiotensin II in the lungs. Angiotensin II functions as a hormone, causing the release of the hormone aldosterone by the adrenal cortex, resulting in increased Na+ reabsorption, water retention, and an increase in blood pressure. Angiotensin II, in addition to being a potent vasoconstrictor, also causes an increase in ADH and increased thirst, both of which help to raise blood pressure.
Key Points
- The hypothalamus monitors the amount of water in the body by sensing the concentration of electrolytes in the blood; a high concentration of electrolytes means that the level of water in the body is low.
- Antidiuretic hormone (ADH), produced by the hypothalamus and released by the posterior pituitary, causes more water to be retained by the kidneys when water levels in the body are low.
- ADH effects water retention by creating special channels for water, called aquaporins, inside the kidneys so that more water can be reabsorbed before it is excreted.
- Aldosterone, produced by the adrenal cortex, causes the retention of water in the body by increasing the levels of sodium and potassium ions in the blood, which causes the body to reabsorb more water.
- When blood pressure is low, the enzyme renin is released, which cleaves the protein angiotensinogen into angiotensin I, which is further converted into angiotensin II.
- Angiotensin II signals the adrenal cortex to release aldosterone, which then increases the retention of sodium ions, enhancing the secretion of postassium ions, resulting in water retention and an increase in blood pressure.
Key Terms
- renin: a circulating enzyme released by mammalian kidneys that converts angiotensinogen to angiotensin-I that plays a role in maintaining blood pressure
- mineralocorticoid: any of a group of steroid hormones, characterised by their similarity to aldosterone and their influence on salt and water metabolism
- electrolyte: any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes
- aquaporin: any of a class of proteins that form pores in the membrane of biological cells
- aldosterone: a mineralocorticoid hormone, secreted by the adrenal cortex, that regulates the balance of sodium and potassium in the body
- osmoreceptor: a sensory receptor primarily found in the hypothalamus of most homeothermic organisms that detects changes in osmotic pressure
- antidiuretic hormone: a hormone secreted by the posterior pituitary gland that regulates the amount of water excreted by the kidneys