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In this article, we will discuss osmoregulation in detail. We will specifically discuss the roles of the hypothalamus, posterior pituitary gland, antidiuretic hormone (ADH), aquaporins, and collecting ducts in osmoregulation. So, let us get started.
What is Osmoregulation?
We can define osmoregulation as:
The control of the water potential of fluids in the body is referred to as osmoregulation.
- Osmoregulation is the fundamental element of hemostasis
- It is critical that the cells are surrounded by tissue fluid that has similar water potential as their own contents so that too much water gain or loss that can potentially disturb metabolism could be prevented.
- It is observed that the water is lost from the fluid inside the nephron as it flows via the collecting duct.
- There can be a difference between the permeability of the walls of the distal convoluted tubule and the collecting duct
- In case of their permeability, the water can move out of the tubule, making the urine concentrated. This water is returned to the blood and retained in the body.
- In case of their impermeability, a small amount of water moves out of the tubule, thus making the urine diluted. A huge amount of water is removed from the body.
The Role of Various Glands and Hormones in Osmoregulation
- Osmoreceptors which are specialized sensory neurons monitor the water potential of the blood. These osmoreceptors are present in the region of the brain called the hypothalamus
- If a decrease in the water potential of the blood is detected by the osmoreceptors, then the nerve impulses are sent along these sensory neurons to the posterior pituitary gland which is another part of the brain found just beneath the hypothalamus
- These nerve impulses trigger the posterior pituitary gland to release a hormone known as antidiuretic hormone (ADH)
- The molecules of ADH enter the blood and move throughout the body
- Due to ADH, kidneys are able to reabsorb more water which in turn reduces the loss of water in the urine
In the next sections of the article, we will discuss ADH in more detail.
Antidiuretic Hormone (ADH)
ADH stands for an antidiuretic hormone that is secreted from the anterior pituitary gland into the blood. If the water potential of the blood is sufficiently low which means that it has a small amount of water in it, then the osmoreceptor cells in the hypothalamus sense it. These osmoreceptor cells are neurons or nerve cells that produce ADH, which travels along their axons and into the anterior pituitary gland from where it is secreted into the blood.
The ADH moves in solution in the blood plasma. It makes the walls of the collecting duct permeable as it reaches them. Hence, the water is reabsorbed from the fluid in the collecting duct and small volumes of concentrated urine are formed.
If the water potential of the blood is high enough which means that the blood has too much water in it, then the osmoreceptor cells sense it and less ADH is secreted. Hence, the walls of the collecting duct become less permeable to water which in turn causes less water to be reabsorbed into the blood. This produces large volumes of diluted urine.
What is Negative Feedback?
The process of controlling the water content of the body using the antidiuretic hormone (ADH) is an example of negative feedback. If the water potential of the blood rises or declines sufficiently, this is sensed by the receptor cells. As a result, effectors are prompted to take any action which causes the water potential to go to the correct value.
In this situation, the osmoreceptor cells in the hypothalamus are receptors, and the endings in the anterior pituitary gland are effectors which secrete ADH.
In the next section of the article, we will discuss how ADH affects kidneys.
How does ADH Affect Kidneys?
- Water gets reabsorbed by the process of osmosis from the filtrate in the nephron
- This reabsorption takes place due to the passing of filtrate through the structures which are referred to as collecting ducts
- Because of the ADH, the luminal membranes which refer to the membranes facing the lumen of the nephron of the collecting ducts become more permeable to water
- ADH achieves this by increasing the number of aquaporins which are the water-permeable channels in the luminal membranes of the collecting duct cells. It takes place in the following way:
- The collecting duct has vesicles. The membranes of the vesicles contain several aquaporins.
- The molecules of ADH bind to the receptor proteins, thus activating a signalling cascade that results in the phosphorylation of the aquaporin molecules
- This causes the activation of the aquaporins which lead to the fusion of vesicles with the luminal membranes of the collecting duct cells
- This enhances the permeability of the membrane to water
- When the filtrate in the nephron moves along the collecting duct, the water molecules travel from the collecting duct (high potential of water), through the aquaporins, and into the tissue fluid and blood plasma in the medulla (low potential of water)
- The filtrate in the collecting duct becomes more concentrated as it loses water
- This leads to the production of a small volume of concentrated urine which flows from the kidneys, via ureters, and into the bladder
In the next section of the article, we will discuss what happens when the water potential of the blood is too high.
What happens if the water potential of the blood is too high?
- When the water potential of the blood is very high, then the exact opposite happens.
- Osmoreceptors in the hypothalamus are not activated
- Nerve impulses are not sent to the posterior pituitary glands
- Due to no nerve impulses, no anti-diuretic hormone (ADH) is released
- Aquaporins move out of the luminal membranes of the cells in the collecting duct
- As a result, the cells in the collecting duct are no longer permeable to water
- The filtrate flows along the collecting duct but does not lose water which implies that it is quite dilute
- This results in the production of a large volume of dilute urine which flows from the kidneys, through the ureters, and into the bladder.
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