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25.1B: Regulation of Water Output

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    8159
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    Fluid can leave the body in three ways: urination, excretion (feces), and perspiration (sweating).

     

    LEARNING OBJECTIVES

     

    Describe the regulation of water output in humans

     

    KEY TAKEAWAYS

    Key Points

     

    • The majority of fluid output occurs from urination. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air.
    • The body’s homeostatic control mechanisms ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (antidiuretic hormone, also known as vasopressin ) and aldosterone play a major role in this.
    • If the body is becoming fluid deficient, increased plasma osmolarity is sensed by the osmoreceptors. This results in an increase in the secretion of ADH that causes fluid to be retained by the kidneys and urine output to be reduced.
    • Aldosterone is the major end-product of the renin – angiotensin system, and increases the expression of ATPase pumps in the nephron that causes an increase in water reabsorption through sodium cotransport.
    • ADH increases water reabsorption by increasing the nephron’s permeability to water, while aldosterone works by increasing the reabsorption of both sodium and water.

     

    Key Terms

     

    • osmoreceptors: Sensory receptors, primarily found in the hypothalamus, that detect changes in plasma osmolarity and contribute to the fluid-balance regulation in the body.
    • anti-diuretic hormone: A neurohypophysial hormone found in most mammals that is responsible for increasing water absorption in the collecting ducts of the kidney nephrons.
    • aldosterone: A corticoid hormone that is secreted by the adrenal cortex that regulates the balance of sodium and potassium and thus the water-balance levels in the body.

     

    Water Output

     

    Fluid can leave the body in three ways:

    1. Urination
    2. Excretion (feces)
    3. Perspiration (sweating)

    The majority of fluid output occurs from urination, at approximately 1500 ml/day (approximately 1.59 qt/day) in a normal adult at resting state. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air; however these fluid losses are considered to be very minor.

    The body’s homeostatic control mechanisms maintain a constant internal environment to ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (anti-diuretic hormone, also known as vasopressin) and aldosterone, a hormone created by the renin–angiotensin system, play a major role in this balance.

    If the body is becoming fluid deficient, there will be an increase in the secretion of these hormones that causes water to be retained by the kidneys through increased tubular reabsorption and urine output to be reduced. Conversely, if fluid levels are excessive, the secretion of these hormones is suppressed and results in less retention of fluid by the kidneys and a subsequent increase in the volume of urine produced, due to reduced fluid retention.

     

    ADH Feedback

     

    When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration of solutes per volume of water. Osmoreceptors in the hypothalamus detect the increased plasma osmolarity and stimulate the posterior pituitary gland to secrete ADH.

    ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption. ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most important compensatory mechanisms during hypovolemic shock (shock from excessive fluid loss or bleeding).

     

    Aldosterone Feedback

     

    Aldosterone is a steroid hormone (corticoid) produced at the end of the renin–angiotensin system. To review the renin–angiotensin system, low blood volume activates the juxtaglomerular apparatus in a variety of ways to make it secrete renin. Renin cleaves angiotensin I from the liver -produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increasing thirst) but it also causes release of aldosterone from the adrenal cortex.

    Aldosterone has a number of effects that are involved in the regulation of water output. It acts on mineral corticoid receptors in the epithelial cells of the distal convoluted tubule and collecting duct to increase their expression of Na+/K+ ATPase pumps and to activate those pumps. This causes greatly increased reabsorption of sodium and water (which follows sodium osmotically by cotransport), while causing the secretion of potassium into urine.

    Aldosterone increases water reabsorption; however, it involves an exchange of sodium and potassium that ADH reabsoption regulation does not involve. Aldosterone will also cause a similar ion -balancing effect in the colon and salivary glands as well.

    This is a diagram overview of the renin–angiotensin system that regulates blood pressure and plasma osmolarity. The hypothalamus of the brain releases a corticotropin-releasing hormone that makes the pituitary gland release ACTH to the liver which, in turn, releases angiotensinogen. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increasing thirst) but it also causes release of aldosterone from the adrenal cortex.

     

    A schematic diagram of the renin–angiotensin system: Overview of the renin–angiotensin system that regulates blood pressure and plasma osmolarity.