Osmoregulation

Definitions & Key takeaways

Osmoregulation is the process by which an organism regulates its internal body water-solute concentrations. It is a crucial aspect of maintaining the proper balance of water and electrolytes in the body, as electrolytes such as sodium, potassium, and chloride are dissolved in water, and a change in their concentrations can affect various physiological processes in the body. Solute concentrations are measured in osmolarity (mOsm/L), which is the number of osmoles within a liter of solution.

In humans, the osmolarity of blood plasma in the body is normally kept around 290 to 300 mOsm/L and is tightly controlled by antidiuretic hormone (ADH). With ADH secretion, the kidney increases the reabsorption of water back into circulation and causes vasoconstriction to bring up blood pressure. These pathways are controlled by negative feedback loops which inhibit further secretion of ADH.

Chapters:

Watch video only

Introduction0:00–0:44

Osmoregulation refers to the regulation of body fluid solute concentrations. Solute concentrations are measured in osmolarity, usually mOsm/L, which is the number of osmoles within a litre of solution.
Now remember that an osmole refers to the individual ions within a solution. For example, a solution of 1 mmol/L of a salt like NaCl which can split apart in water to become Na+ and Cl- will have both Na+ and Cl- contribute to the osmolarity.
So 1 mmol/L of NaCl is 2 mOsm/L. In a normal body, blood plasma osmolarity is very tightly regulated and kept at around 290 to 300 mOsm/L.

Osmolarity0:44–1:55

The main components of this osmolarity is made up of ions like sodium, glucose, and urea. To get the actual osmolarity of the body, a calculation like this one can be used: = 2[Na+] + [Glucose]/18 + [ BUN ]/2.8, where [Glucose] and [BUN] are measured in mg/dL.
Both glucose and BUN can be converted from mg/dl to mOsm/L by dividing them by 18 and 2.8 respectively. Let’s say that it's a super sunny day out and you forget to bring water with you.
Well first, as you walk around, you’re constantly losing water through sweat as well as water vapor from your mouth and nose as you breathe out - these are insensible water losses.
Without drinking water, you can quickly get dehydrated. This causes your plasma osmolarity to increase, because the fluid levels in your blood drop, but the total number of solute particles in remains roughly the same.

Osmoreceptors1:55–2:50

Two things now begin to happen simultaneously. First, a region in the brain called the anterior hypothalamus has a cluster of neurons called supraoptic nuclei, which have osmoreceptors that sense even tiny changes in osmolarity, as small as 1 mOsm/L.
These neurons are always sampling the blood that passes by. With increases in plasma osmolarity, water will flow out of the cell causing it to contract.
Increases in osmolarity past the normal set point of 290 to 300 mOsm/L stimulates the hypothalamus to produce antidiuretic hormone or ADH - also called vasopressin.
Second, as the blood volume drops, so does the blood pressure. Specialized neurons, called baroreceptors, act as pressure sensors in the walls of the cardiovascular system - in a few specific areas.

Baroreceptors2:50–3:44

They’re in the posterior wall of the right atria of the heart, in the aortic arch, and in the right and left carotid sinuses, which is where the common carotid splits to become the internal and external carotid.
These baroreceptors detect tiny changes in how stretched out those walls are, so if blood volume decreases and there’s less stretch on those walls, the baroreceptors change their rate of firing a signal up to the hypothalamus.
The hypothalamus senses the change and starts making more antidiuretic hormone. So ultimately both an increase in osmolarity and a decrease in pressure leads to more ADH.

Antidiuretic hormone (ADH)3:44–4:47

Antidiuretic hormone is peptide hormone - a small protein that cells use to communicate with one another. ADH is made within the cell bodies of supraoptic neurons, and then gets packaged into vesicles and gets secreted down long axons which extend into a synaptic cleft in the posterior pituitary.
The ADH gets released into the interstitial fluid, moves through nearby endothelial cells, and gets into the capillary bed of the posterior pituitary gland.
From there, the ADH travels throughout the body and binds to receptors in its two main target tissues, the collecting ducts of the kidney, and the smooth muscle that wraps around arterial walls.
Now, starting with the kidney, the functional unit of the kidney is the nephron, and the collecting ducts connect those nephrons to the minor calyx of the kidney.
This collecting duct part is normally impermeable to water and urea. ADH acts on the principle cells that are found along the collecting ducts.

Principal Cells4:47–5:44

These cells have two sides, the apical or luminal side, also known as the side in contact with the tubular fluid and the basolateral or interstitial side, the side that is in contact with the interstitium of the kidney.
ADH travels through the peritubular capillaries of the kidneys and binds to V2 receptors on the basolateral membrane of the principal cell.
Once the V2 receptors are bound, the principle cells incorporate water protein channels called aquaporins in the luminal membrane of the cell.
Because the solute concentration in the interstitium is high, water flows via osmosis, from the lumen of the tubule down its concentration gradient, into the interstitium.
From there, water can also freely enter the peritubular capillaries so that it can be reabsorbed back into systemic circulation.
More water in the systemic circulation decreases plasma osmolarity Now, looking at those smooth muscles in the walls of blood vessels, ADH also causes causes them to contract.

Resistance5:44–6:31

As the diameter of the blood vessel lumen decreases, the blood pressure will increase. If we look at the relationship between radius of a tube and the resistance, we know that resistance is proportional to 1 over the radius to the fourth power.
And because pressure or delta P equals resistance x flow, an increase in peripheral resistance causes an increase in pressure.
As the osmolarity normalizes and blood pressure rises, both osmoreceptors and baroreceptors stop stimulating the anterior hypothalamus, and as a result less ADH is secreted.

ADH Regulation6:31–7:58

Now let's consider a different situation. Let’s say that you start drinking a lot of water - way more than what you usually drink.
That extra fluid diffuses through the large intestines and gets into the blood and decreases the plasma osmolarity. This decrease in plasma osmolarity inhibits osmoreceptor firing from the hypothalamus which inhibits ADH secretion.
As less ADH reaches the kidney, aquaporin protein channels don’t get incorporated into the apical or luminal surface of the principal cells and water reabsorption can’t occur.
As more water is excreted in the urine, you end up going to the bathroom a lot more. As water gets removed by the urine, plasma osmolarity increases back to normal.
Second, which happens sort of at the same time as the first, more fluid increases plasma volume which stretches the walls of blood vessels, and baroreceptors sense that stretch and also causes the hypothalamus to stop ADH secretion.
Without ADH, smooth muscles relax, and this results in the radius increasing, the the resistance decreasing, and therefore there’s a drop in blood pressure.
So ADH inhibition causes both the removal of excess water and the relaxation of blood vessels, which work together to help return blood osmolarity and volume back to normal.
OK, as a quick recap, osmolarity of blood plasma in the body is normally kept around 290 to 300 mOsm/L and is tightly controlled by ADH.

Review7:58–8:24

With ADH secretion, the kidney increases reabsorption of water back into circulation and causes vasoconstriction to bring up blood pressure.
Both pathways are controlled by negative feedback loops which inhibit further secretion of antidiuretic hormone.