Osmoregulation is the process by which the absorption and loss of water and solutes are balanced.
Just as thermoregulation is based on balancing heat loss and gain, controlling the chemical composition of bodily fluids is based on balancing water and solute absorption and loss.
Animal cells swell and burst when water intake is high; when water loss is significant, cells shrivel and die. Finally, a concentration gradient of one or more solutes across the plasma membrane drives the flow of both water and solutes in animals, as it does in all other creatures.
The image attached shows the association between solute concentration and osmosis.
Water balance may be maintained by an animal in two ways. One is to be an osmoconformer, which is to be isoosmotic with its environment. Osmoconformers are all marine creatures. There is no propensity for an osmoconformer to acquire or lose water since its internal osmolarity is the same as that of its surroundings.
Many osmoconformers survive in water with a steady composition and, as a result, a consistent internal osmolarity.
The second approach to keep the water balanced is to be an osmoregulator, which means controlling internal osmolarity independently of the external environment. Osmoregulation allows animals to exist in conditions that osmoconformers cannot, such as freshwater and terrestrial habitats, or to travel
Water enters and exits cells via osmosis, which happens when the total solute concentration of two solutions separated by a membrane differs (as shown in the attached image). Solute concentration is measured as osmolarity, which is the number of moles of solute per liter of solution. Human blood has an osmolarity of around 300 milliosmoles per liter (mOsm/L), whereas saltwater has an osmolarity of about 1,000 mOsm/L.
Isoosmotic solutions are those that have the same osmolarity. Water molecules will constantly traverse a selectively permeable barrier that separates the liquids.
Most animals, whether osmoconformers or osmoregulatory, cannot withstand significant fluctuations in external osmolarity and are referred to be stenohaline (from the Greek stenos, narrow, and halos, salt). euryhaline animals (from the Greek euros, wide) can, on the other hand, withstand huge variations in external osmolarity.
Barnacles and mussels in estuaries that are alternately exposed to fresh and saltwater are examples of euryhaline osmoconformers; striped bass and different salmon species are examples of euryhaline osmoregulation (as shown in the image attatched below).
Following that, we'll look at osmoregulation adaptations that have developed in marine, freshwater, and terrestrial species.
The image attached below shows osmoregulation in marine and freshwater bony fishes: a comparison.
Selective secretion and reabsorption in the proximal tubule of the nephron change the amount and content of the filtrate.
The loop of Henle's descending limb is permeable to water but not salt; water flows into the interstitial fluid via osmosis.
The ascending limb is salt permeable but not water permeable; salt exits by diffusion and active transport. The distal tubule and collecting duct regulate the amounts of K+ and NaCl in bodily fluids.
In mammals, the gradient of salt content in the kidney interior is maintained via a countercurrent multiplier system including the loop of Henle. Urea leaving the collecting duct adds to the kidney's osmotic gradient.
Natural selection formed the foreground.
When blood osmolarity exceeds a certain threshold, such as when water intake is insufficient, the posterior pituitary gland secretes antidiuretic hormone (ADH). ADH increases the number of epithelial aquaporin channels in the collecting ducts, which improves their permeability to water.
When the afferent arteriole's blood pressure or volume declines, the juxtaglomerular apparatus releases renin.
Angiotensin II, which is produced in reaction to renin, constricts arterioles and causes the release of the hormone aldosterone, rising blood pressure, and decreasing renin release. This renin-angiotensin-aldosterone system shares functions with ADH and is inhibited by the atrial natriuretic peptides.