Thin descending LOH - Does it have active transport of Na+ - Is it permeable to water, NaCl, and Urea

- No active transport - Permeable to water, NaCl, urea (everything is normally passive

Thin ascending LOH - Is there an active transport for NaCl - Is it permeable to water, NaCl, urea?

- No active transport to NaCl - Impermeable to water - Permeable to NaCl and urea

Thick ascending LOH - Does it have active NaCl transport - Is it permeable to water and urea?

- Has active NaCl transport capable of establishing a 200 mOsm/L concentration grandient - Impermeable to water and urea

Renal-Chapter 29 Flashcards by Mary Miller

What are the ranges of urine osmolarity in cats and dogs?

Dog: 50-2400 mOsm/L
Cat:50-3300 mOsm/L

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An increase in ADH would have what effect on urine?

More concentrated urine

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A decrease in ADH would have what effect on urine?

More dilute urine

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Give renal mechanism for excreting dilute urine (normal conditions)
-Does body excrete xs amount of solutes?

After water ingestion, 30 min later, it gets absorbed.

Urine flow rate increase

Urine osmolarity decrease

Excretion of a large volume of dilute urine

Total amount of solute excreted and plasma osmolarity remain relatively constant. Body does not excrete xs amount of solutes.

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Give renal mechanism of dilute urine excretion when ADH levels are very low
-What parts are sensitive to ADH?

Tubular fluid remains isosmotic in PT

Descending LOH tubular fluid becomes more concentrated as it flows into the inner medulla

Ascending LOH tubular fluid is diluted (regardless if ADH is present or not)

Tubular fluid in DT and CT is further diluted in the absence of ADH

CT are sensitive to ADH
ALOH is not sensitive to ADH

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In general, how do kidneys conserve water if there is water deficit?

Excrete concentrated urine

Excrete solute and reabsorb water

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Which species would have higher urine osmolarity threshold? Beavers or desert species. Why?

Desert species=10,000 mOsmoles/L
Beaver- 500 mOsmoles/L

Desert species have a higher urine concentrating capacity and more juxtamedullulary nephrons to converse water in drier environment.

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How much concentrated urine must a human excrete a day?

-What does excretion consist of?

600 mOsm

Waste products of metabolism
Ingested solutes

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What is formula for obligatory urine volume?

Mandatory concentrated urine to be excreted/Maximum urine concentrating ability

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The higher the concentrating ability, obligatory urine volume is
Higher or lower?

Lower`

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If you drank 1 L sea water of 1200 mOsm/L how would you compensate for that?

Automatically have to get rid of 600 mOsm/L but you’ve ingested 1200 mOsm of NaCl water.

600+1200= 1800 mOsmol to get rid of

1800/1200 (max urine concentration ability)

You’ve have to drink 1.5 L of water to compensate dehydration.

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What does urine specific gravity measure?

estimates urine solute concentration ability

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How is urine specific gravity different from osmolarity?

Specific gravity takes into account the number and SIZE of the solute molecules.

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What can alter urine specific gravity?

Large molecules like glucose and AB can give false results suggesting that the urine is very concentrated

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What are normal values of urine specific gravity for humans, dogs, cats

Humans: 1.002-1.028
Dog:1.001-1.070
Cat:1.001-1.080

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Requirements for excreting concentrated urine

High level of ADH

High osmolarity of the medullary interstitium

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Why does there need to be a high level of ADH for excreting concentrated urine?

ADH causes water reabsorption at a greater rate than solute reabsorption thus creating concentrated urine

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Why is a high osmolarity of medullary interstitium necessary for excreting concentrated urine?

Interstitium osmolarity of cortex=300 mOsm/L
medulla=1200-1400 mOsm/L (more concentrated)

Osmotic gradient necessry for water reabsorption…

Use countercurrent mechanism

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T/F Concentrated urine depends on the anatomical arrangement of LOH

True

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T/F Collecting ducts move through medulla and contain filtrate from single nephron

Contains filtrate from multiple nephrons

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Thin descending LOH

Does it have active transport of Na+
Is it permeable to water, NaCl, and Urea

No active transport

- Permeable to water, NaCl, urea (everything is normally passive

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Thin ascending LOH

Is there an active transport for NaCl
Is it permeable to water, NaCl, urea?

No active transport to NaCl
Impermeable to water
Permeable to NaCl and urea

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Thick ascending LOH

Does it have active NaCl transport***
Is it permeable to water and urea?

Has active NaCl transport capable of establishing a 200 mOsm/L concentration grandient
Impermeable to water and urea

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Explain how the countercurrent multiplier system in LOH produces hyperosmotic renal medulla

As fluid moves through the loop, Na and Cl is pumped out of the ascending limb raising interstitial fluid osmolarity UP TO 200 mOsm/L GRADIENT.

Water then moves from descending LOH by osmosis and concentrates filtrate.

This repeats until ma is reached (~1200 mOsm/L) at deepest medullary point.

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When do cortical collecting ducts become high permeable to water?

After passage through LOH and HIGH ADH levels

Explain role of collecting ducts in excreting concentrated urine

Water is reasborbed into cortical interstitium and carried away by peritubular capillaries Most of water reabsorbed in corte helps preserce medullary interstitial osmolarity Further water reabsorption in medulla but small compared to cortex.

T/F Urea contributes to the hyperosmotic renal medullary interstitium. If so when?

T About 40 percent (500 mOsm/L) When kidney forms maximum concentrated urine

How is urea reabsorbed in MCD?

Stimulation of ADH Urea will be passively reabsorbed by facilitated diffusion through urea transporters

T/F DT and CCD are permeable to urea

F They are impermeable

Outline the flow of urea through tubules when ADH is high

50 percent is immediately reabsorbed (at proximal tubule) Concentration increases through LOH and water is reabsorbed faster DT/CCD impermeable to urea but water moves out Since ADH is present, MCD is permeable to urea Urea diffuses down concentration gradient into interstitial fluid and re-enters and recirculates to help maintain concentration gradient

T/F Countercurrent exchange in the vasa recta preserves hypoosmolarity of renal medulla

Preserves HYPEROSMOLARITY in renal medulla

T/F Medullary blood flow is high. Higher than 5 percent of total kidney flow

False Medullary blood flow is low, less than 5 perent of total kidney flow

Medullary blood flow advantages (2)

Sufficient to supply metabolic needs of tissue Minimzes solute loss/washout

What area acts as a countercurrent exchange

Vasa recta

Explain the countercurrent exchange in the vasa recta

Plasma flowing down the descending LOH of the vasa recta becomes more HYPEROSMOTIC (due to diffusion of water out of the blood and diffusion of solutes from renal interstitial fluid into the blood) In the ascending LOH of the vasa recta, solutes diffuse back into the interstitial fluid and water diffuses back into the vasa recta.

Why and where does the environment become HYPEROSMOTIC during countercurrent exchange in the vasa recta?

Descending LOH Because diffusion of water out of blood and diffusion of solutes from renal interstitial fluid into the blood. Water is being pulled out of tubule and exchange of solutes/H2O is possible due to slow blood flow in this area.

ADH causes an increase or decrease of osmolarity of tubular fluid

INCREASE

What are the two primary mechanisms for ECF Na+ and osmolarity regulation?

Osmosreceptor-ADH system Thirst mechanism

How can you estimate plasma osmolarity from plasma Na+

P(osm)= 2.1 X Plasma Na+

Where is ADH made?

Neurons of hypothalamus

What releases ADH?

Posterior pituitary

Explain how osmosreceptor-ADH system works

There's a water deficit Increase ECF osmolarity Osmoreceptors SHRINK and there's increase in ADH secretion Increase in plasma ADH Increase in water permeability in DT and CT Increase water reabsorption Decrease water excretion

What are two cardiovascular reflexes also have effect on ADH release

Arterial baroreceptor Cardiopulmonary reflex

What does arterial baroreceptor reflex monitor

Pressure changes

What does the cardiovascular reflex monitor? | -What are 2 features

Monitor volume changes Afferents into sensory area Projections to hypothalamus

An increase in ADH would have what effect on arterial pressure, blood volume, and urine

Decrease in arterial pressure Decrease in blood volume Urine is decreased flow and concentrated

Is ADH release mechanism more sensitive to osmotic stimuli or pressure/volume stimuli?

Osmotic stimuli

Would nausea, vomiting, nicotine, and morphine stimulate or inhibit ADH release?

Stimulate Want to retain more water

Would alcohol and caffeine inhibit or stimulate ADH release?

Inhibit ADH release (diuretics)

Would ingesting water increase or decrease ADH release?

decrease

Nausea effects... - ADH - Blood volume - Blood pressure - Plasma osmolarity

Increase ADH Decrease blood volume Decrease pressure Increase plasma osmolarity

Increase thirst (dryness of mouth) effects - Plasma osmolarity - Blood volume - Blood pressure - Angiotensin II

Increase plasma osmolarity Decrease blood volume Decrease blood pressure Increase angiotensin II

Decrease thirst (gastric distention) effects - Plasma osmolarity - Blood volume - Blood pressure - Angiotensin II

- Decrease osmolarity - Increase blood volume - Increase blood pressure - Decrease angiotensin II

T/F The area along AV3V that promotes ADH release also stimulates thirst and involve the same nuclei

F Same area but involves different nuclei

What are some stimuli for thirst?

Increase ECF osmolarity

Another name for anteroventral region of the third ventricle (AV3V)

Thirst center

Electrical stimulation of AV3V center induces what type of behavior

Drinking behavior

Injection of hypertonic salt solution stimulates what type pf behavior

Thirst

Outline stimuli for thirst mechanism

There's increased ECF osmolarity due to increased plasma Na+ concentrations, causing intracellular dehydration in the thirst centers Decreases in ECF volume and arterial pressure Angiotensin II acts on subfornical organ to stimulate thirst and on kidney to increase Na+ and water reabsorption (in response to low pressure/volume) Dryness of mouth and membranes

Excessive thirst is called

polydipsia

Diabetes mellitus - osmolarity - urine output - prevalent in

High concentrations of glucose and causes increase in osmolarity Increase urine output Increase water excretion Increase thirst More prevalent in older animals More prevalent that diabetes insipidus

Diabetes insipidus | -2 types

Central diabetes insipidus Nephrogenic diabetes insipidus

Central diabetes insipidus - Problem - Origin - Rx

Inability to produce or release ADH May be congenital or injury-induced Treatment-synthetic ADH, desmopressin

Nephrogenic diabetes insipidus - Problem - ADH

Renal tubules excrete dilute urine-which may be due to failure of countercurrent mechanism to to form hyperosmotic medulla or inability to respond to ADH. ADH is normal Can be caused by diuretics, lithium, tetracyclines, or renal diseases that damage renal medulla

What is "meter" fluid intake?

Thirst that is relieved immediately after drinking- before water has been absorbed.

Distention of the GI tract can relieve what? | How is this beneficial?

Relieve thirst Prevents over-hydration

T/F Animals drink almost exactly the amount necessary to return plasma osmolarity to normal.

When is the thirst mechanism activated? | What is this also known as

When Na+ concentration is increased 2 mEq/L above Threshold for drinking

Explain the relationship of the integrated responses of Osmoreceptor-ADH and thirst mechanism - What do they both do - If one fails - If both fails

Osmoreceoptor-ADH and Thirst mechansm both work to regulate osmolarity. If one fails, the other can ordinarily control osmolality If both fail, there s no mechanism to increase water ingestion or conserve water

T/F Angiotensin II and aldosterone have potent effects on renal Na+ reasbsorption/excretion

Low Na+ intake stimulates or decreases ang II and aldosterone formation?

Low intake of Na+ stimulates angiotensin II and aldosterone formation.

T/F Angiotensin II and aldosterone have ptent effect on ECF Na+ concentrations. Why?

F They increase both sodium and water reabsorption...so volume changes but concentration does not ADH-thirst mechanism compensates

The normal ECF volume and sodium concentration is a balance between

Sodium excretion Sodium intake

What are 2 major stimuli that increase salt-appetite

Decreased sodium concentration in ECF Crculatory insufficiency (often caused by decreased blood volume or blood pressure)

T/F Salt appetite it thought to be under control of neuronal mechanisms similar to thirst