Renal Flashcards

1
Q

Regarding osmoregulation, describe the “osmoconformer” strategy.

A

An osmoconformer is an animal that matches the environment while maintaining cellular function.

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2
Q

Regarding osmoregulation describe the “osmoregulator” strategy

A

An osmoregulator is an animal that maintains tight control of its internal environment regardless of outside conditions.

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3
Q

Are osmoregulation and osmoconformation mutually exclusive?

A

No. An organism can have some mechanisms under regulatory control and some not.

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4
Q

What are some mechanisms under regulatory control?

A

Osmotic regulation (maintaining total dissolved solutes for osmo pressure), ionic regulation, volume regulation

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5
Q

What is one way to identify an osmoconformer versus an osmoregulator on a graph?

A

Plot blood osmotic pressure and ambient osmotic pressure. An osmoconformer will have a visible increasing slope, an osmoregulator will remain relatively constant. This also shows those with mixed systems.

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6
Q

What are the challenges of freshwater regulators?

A

Freshwater regulators live in a hypo osmotic environment and thus they struggle to maintain needed ions and rid excess water.

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7
Q

What are the challenges of marine regulators?

A

Marine regulators live in a hyperosmotic environment and thus they struggle to rid excess ions and keep water.

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8
Q

What is the main surface of aquatic ion exchange?

A

The gills. They have a high surface area to meet oxygen demands and thus are also key to the intake/loss of water and ions.

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9
Q

What are the important cells of the gill?

A

Pavement cells which make up most of the gill’s surface, Mitochondria rich cells (mRc) which maintain internal [solute], and chloride cells/ionophores. Accessory cells are also important but exclusively found in marine fish.

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10
Q

What is the role of a pavement cell in a gill?

A

It is the main site of oxygen exchange and makes up 90% of the gill.

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11
Q

What is the role of an MRC in a gill?

A

MRCs deal with ion loading challenges and will uptake Chloride, Sodium, and Calcium ions in freshwater and remove Chloride and Sodium ions in saltwater. It is under hormonal control partially and the density and type of MRCs can change depending on the external environment.

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12
Q

What is one way MRCs change in response to different conditions?

A

In soft water there is low calcium, thus calcium from within the organism will want to diffuse out because of concentration gradients. Thus, the organism will have more and larger MRCs to take up more calcium because of the calcium that is lost.

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13
Q

What role does active transport play in MRCs?

A

In freshwater MRCs actively transport ions into the organism, and in saltwater MRCs actively transport ions out of the organism. This is active transport because it is against a concentration gradient.

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14
Q

Describe the role of V-type ATPase in the gills.

A

In freshwater gills, it constantly pumps out protons using ATP on the apical membrane of MRCs. This attracts sodium ions due to a net negative charge.

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15
Q

Describe the role of Na/K ATPase in the gills.

A

In freshwater gills, it exchanges 3 sodium to the blood for 2 potassium into the cell which leaks back out into the blood by leak channels, this further adds to the negativity. It is in the basolateral membrane of MRCs. It is the same in marine gills.

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16
Q

Describe the role of the electroneutral anion exchanger in the gills.

A

In freshwater gills, it exchanges bicarbonate waste for chloride. It’s in the apical membrane of pavement cells and MRCs. The binding of bicarbonate causes a conformation change that has a strong chloride binding site. It is either not present in marine gills or not worth mentioning.

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17
Q

Describe the role of the Cystic Fibrosis Transmembrane Regulator in the gills.

A

In freshwater gills, it’s a chloride channel that is not active transport. It is in pavement cells and MRCs, and its driven by the eventual build up of chloride becoming so high it is pushed through the CFTRs into the blood. Mutations cause cystic fibrosis, which reduces chloride clearance, maintains high electroneg potential, reduces extracellular cation removal, and increases mucosal build up (tissue water retention) leading to resp and digest difficulties. It is either not present in marine gills or not worth mentioning.

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18
Q

Describe the role of the calcium co-transporter and calcium ATPase in the gills.

A

In freshwater gills, the calcium co-transporter relies on the gradient established by the NA/K ATPase to exchange a sodium into the cell for a calcium into the blood. It is on the basolateral membrane of MRCs. Calcium ATPase is also on the basolateral membrane and actively transports calcium into the blood. It has the same role in marine gills.

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19
Q

Why does drinking seawater dehydrate you?

A

Because the salt water is hyperosmotic to your blood plasma, and thus the water in your blood plasma is drawn into the salt water in your gut and sodium and chlorine will diffuse into the blood plasma.

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20
Q

How do saltwater fish differ from mammals in their ability to drink sea water?

A

They have active transport mechanisms for sodium and chloride into the blood plasma later in their intestine, this allows water retention but keeps a lot of excess ions which have to get removed via ion exchange mechanisms in the gills.

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21
Q

What is the role of the accessory cell in the gills?

A

In saltwater fish exclusively it has a tight junction to the MRC and it created a paracellular path for sodium, which is moved through the path by electromotive forces.

22
Q

What is the role of the NKCC cotransporter in the gills?

A

In saltwater fish, it transports one sodium, one potassium, and two chloride into the cell using the very high attractive force for sodium (maintained by sodium ATPase). Eventually enough chloride builds up it diffuses out of channels on the apical membrane. It is on the basolateral membrane of MRCs. It is not present in freshwater fish.

23
Q

Identify these gill ion transporters by whether they are present in marine, freshwater, or both types of fish. Also describe their function and location in a couple of words.
1. V-type ATPase
2. Na/K ATPase
3. Electroneutral anion exchangers
4. Cystic Fibrosis Transmembrane Regulators
5. Calcium co-transporters
6. Calcium ATPase
7. Paracellular sodium pathway
8. NKCC cotransporter

A
  1. Freshwater. Apical membrane of MRCs. Proton pump (out of organism). Maintains negative charge in cell
  2. Both. Basolateral membranes of MRCs. Exchange 3 sodium to blood for 2 potassium into cell. Further maintain membrane potential.
  3. Freshwater. Apical membrane of pavement cells and MRCs. Exchange equal negative charges. Usually bicarb out, chloride in. Builds up chloride.
  4. Freshwater. Pavement cells and MRCs. Huge buildup of chloride drives diffusion through these channels into the blood.
  5. Both. Basolateral membrane of MRCs. Transports a sodium into the cell and a calcium into the blood. Relies on gradient established by Na/K ATPase.
  6. Both. Basolateral membrane of MRCs. Actively transports calcium into the blood.
  7. Marine. Between the accessory cell and the MRC. Provides a pathway for sodium to exit the cell driven by electromotive forces.
  8. Marine. Basolateral membrane of MRCs. Transports 1 sodium, 1 potassium, 2 chloride into the cell. Driven by Na/K ATPase gradient to use sodium’s attraction force to also move the other ions. Eventually chloride builds up enough to leak out of diffusion channels on the apical membrane.
24
Q

How do marine birds and reptiles deal with osmoregulation challenges?

A

Salt glands in the nose/head secrete salt. Blood vessels close to the secretory cells secrete salt into collecting tubules which drain into a duct and are excreted through the nostrils. They work similarly to marine gills and have a paracellular pathway, Na/K ATPase, and NKCC cotransporters. If they drink salt water they will also have exchangers in the gut to retain water similar to saltwater fish.

25
Q

How do the elasmobranchii osmoregulate?

A

They are osmoconformers that maintain the same total concentration of solutes to the environment, but not the SAME solutes, mostly organic ones like urea and TMAO. They don’t have to struggle with losing or gaining water as much.

26
Q

How do salmon osmoregulate?

A

Born in fresh, migrate to salt, move back to fresh. They spend time in brackish waters with salinity gradients and thus slowly acclimate. They also reduce or increase their water consumption as needed. Their kidney function also changes to produce concentrated or dilute urine and their MRCs will either take up or remove ions dependent on their environment, this proves that MRCs are recycled and can change.

27
Q

What are some sources of water loss for terrestrial organisms?

A

Respiratory water loss, evaporative water loss (depending on environment), excretory water loss (removing metabolic products (i.e. urine))

28
Q

How does respiratory water loss work? What are some ways terrestrial organisms combat it?

A

Our respiratory organs have large surface area for gas exchange and the surface is moist and prone to water loss, this is counteracted by having mostly internal respiratory systems. Additionally, our body temperature is warmer than the surrounding air and warmer air holds more water, so external air coming in is humidified and air leaving cools and wets the nose.

29
Q

What factor causes evaporative water loss to vary?

A

SA/V ratio. Smaller animals have larger evaporative water loss by mass due to more volume per SA unit, whereas larger animals have lower evaporative water loss by mass due to less volume per SA unit.

30
Q

How do we combat excretory water loss?

A

By changing the composition of urine.

31
Q

What is the U/P ratio?

A

The ratio of urine osmotic pressure to plasma osmotic pressure. It can be used to show how concentrated or dilute urine is compared to the blood.

32
Q

What is the role of the mammalian kidney in osmoregulation?

A

It produces urine in different concentrations and volumes, it regulates water loss and it regulates solute concentrations.

33
Q

What is the functional unit of urine concentration?

A

The nephron.

34
Q

What is primary urine?

A

Fluid that has just moved from the renal corpuscle into bowman’s capsule (collectively known as the glomerulus). It will change in composition before being excreted as definitive urine and has similar concentration to the blood plasma.

35
Q

What drives the flow of fluid into Bowman’s capsule?

A

Hydrostatic pressure! Blood pressure is the highest contributor and is positive and opposed by colloid osmotic pressure (more solutes in plasma b/c large proteins cannot pass into capsule) and capsular fluid hydrostatic pressure (capsule like balloon. Doesn’t want more fluid). Overall positive, fluid moves into capsule.

36
Q

Describe the ultrafilter of the renal corpuscle.

A

Capillaries: Fenestrations allow small things to diffuse, excluding large proteins.
Basement membrane: collagen protein, further preventing large proteins from escaping.
Podocytes: a specialized epithelial cell extending from the central cell body that forms a mesh preventing large cells from passing.

37
Q

What is glomerular filtration rate?

A

The rate of production of primary urine and the overall amount of fluid moving from blood across all nephrons. It is relatively constant.

38
Q

Define the two types of nephrons and highlight their differences.

A

Cortical nephrons: closer to the renal cortex, with a short loop of henle that doesn’t descend far.
Long loop nephrons: less common and descend far into the medulla. These concentrate urine more than cortical nephrons.

39
Q

How does the thickness of the renal medulla connect with an animal’s ability to concentrate urine?

A

A thicker renal medulla = more + longer long loops of Henle, allowing more concentrated urine to be produced.

40
Q

How does permeability vary across the loop of Henle?

A

Thin descending: highly permeable to water, moderately permeable to solutes
Thin ascending: impermeable to water, moderately permeable to solutes
Thick ascending: impermeable to water, active transport of NaCl into interstitium.

41
Q

How does active transport in the thick ascending loop of Henle work?

A

There’s an NKCC cotransporter from the lumen to the cell and a paracellular pathway for sodium from the lumen to the interstitium. Na/K ATPase transports sodium into the interstitium from the cell and chloride when built up from NKCC diffuses into the interstitium.

42
Q

How does the single effect work?

A

It’s an initial osmotic pressure gradient established in the loop of Henle’s ascending and descending limb based on their permeabilities. Since the descending loop is permeable to solutes and water and the ascending loop is impermeable to water and actively transports out sodium and chloride, we end up with a highly concentrated insterstitium and descending loop and a low concentrated ascending loop which creates a transverse osmotic pressure gradient called the single effect!

43
Q

Describe how countercurrent multiplication works.

A

Essentially given the properties of the single effect, these osmotic pressure differences are multiplied since the fluids are moving in different directions through the nephron. It creates an axial concentration gradient with super high concentration in the inner medulla and lower concentration closer to the cortex of the interstitial fluid.

44
Q

Describe how (and why) the permeability of the collecting duct changes.

A

Antidiuresis: concentrated urine. The collecting duct is permeable to water, so due to the axial concentration gradient water exits the duct into the interstitium.
Diuresis: Dilute urine. The collecting duct is impermeable to water, so water cannot exit the duct into the intersitium.
This is controlled by ADH which causes insertion or removal of Aquaporin-2 (via its absence or presence, its presence inserts, its absence removes).

45
Q

What stimulates the release of ADH?

A

ADH release is stimulated by low levels of blood plasma (water retention and concentrated urine needed). It’s detected by baroreceptors in large blood vessels and osmoreceptors in the hypothalamus. Osmoreceptors detect blood osmolality, if plasma is dilute then they swell because of greater osmoreceptor concentration which triggers a decrease in ADH release and vice versa in the reverse scenario.

46
Q

How does Aquaporin-2 insertion and removal in the collecting duct work?

A

Vasopressin receptors (V2R) are activated by the binding of vasopressin (ADH) to it. It is a g-coupled receptor which triggers the activation of adenylyl cyclase and stimulates PKA to cause the exocytosis of aquaporin-2 from aquaporin water containing vesicles (AQWCV) and the insertion of them into the collecting duct membrane. In the absence of ADH, PKA is inhibited and it triggers the endocytosis of AQ into AQWCVs.

47
Q

What is urea?

A

Nitrogenous waste converted from ammonia to keep blood pH from changing due to ammonia.

48
Q

How does urea permeability change across the nephron?

A

Low permeability: distal convoluted tubule, thick ascending segment of loop of Henle, cortical and outer renal medulla
High permeability: collecting duct and inner renal medulla.

49
Q

How does urea transporter protein function?

A

Urea transporter proteins transport urea from the collecting duct into the interstitium, because of this high concentration it flows into the lowest parts of the loop of Henle. It’s powered by positive feedback. It’s up and downregulated by ADH. It’s called UT.A1

50
Q

How does the blood supply to the renal medulla avoid losing water, gaining ions, and ruining the single effect?

A

The Vasa Recta is a collection of very thin and small arterioles that travel to the deepest parts of the medulla to supply their needs. There is very little bloodflow and countercurrent exchangers to minimize solute washout and preserve osmotic pressure gradients. It functions similarly to the loop of Henle in how solutes move in and out. Additionally, since it’s net osmolarity is higher due to plasma proteins there’s a net loss of water from the interstitium to the blood!