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18 Cards in this Set

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How kidneys conserve water

The kidney conserves water (by excreting less water) through its ability to produce small volume of urine that is more concentrated than plasma. This is accomplished through countercurrent multiplication in the loop of Henle that provides the osmotic force for water reabsorption from the lumen of the collecting duct.

Counter current system

A system with two parallel and adjacent tubes separated by a membrane of finite permeability and within which the flow of the fluid is in the opposite direction.

Countercurrent exchanger

PASSIVE system, producing equilibrating effect at each horizontal level between two adjacent tubes with opposing flow, therefore it helps intensify as well as maintain pre-existing vertical gradient. It does NOT create any gradient.


Vasa recta is an example of countercurrent exchanger.

Countercurrent multiplier

Possesses an energy source (active process) to generate a horizontal concentration gradient between two adjacent tubes. This horizontal gradient is then multiplied vertically along the length of the tube as the fluid flows through. Countercurrent multiplier can both generate and maintain the gradient that it creates.


The loop of Henle in the kidney is an example of countercurrent multiplier.

Countercurrent multiplication in the loops of Henle: permeability characteristics of the nephron.

Proximal tubule: highly permeable to salts AND water.


Descending limb of loop of Henle: relatively impermeable to salts and VERY permeable to water.


Ascending limb of loop of Henle: low water permeability but permeable to salts. Na and Cl are actively reabsorbed in the thick ascending limb, but passively reabsorbed in the thin ascending limb.


Distal tubule and collecting duct: permeable to salts, low water permeability in the absence of ADH but permeable in the presence of ADH.

Operation of the countercurrent multiplication system in the loop of Henle.

Causes:


Fluid in ascending limb of loop of Henle to become progressively diluted.


As osmotic gradient to be established both within the descending limb as well as in the medullary interstitium.

Countercurrent multiplication: after established medullary osmotic gradient, the following occurs as new filtrate flows down the nephron.

1. Fluid in proximal tubule is isosmotic to plasma.


2. Fluid in descending limb of loop of Henle becomes progressively concentrated and fluid in ascending limb of loop of Henle becomes progressively diluted.


3. Formation of hypo-osmotic (dilute) urine: low or zero circulating level of ADH in distal tubule and collecting ducts; large volume of dilute urine is excreted.


4. Formation of hyper-osmotic (concentrated) urine: high circulating level of ADH causes distal nephron to become permeable to water (by inducing insertion of water channels into apical membranes); small volume of concentrated urine is excreted.

Role of Urea in countercurrent system

Deposition of urea in the medullary interstitium. High medullary urea occurs through medullary recycling of urea. Urea helps establishing medullary osmotic gradient with less energy expenditure.


Urea is only permeable in the inner medullary segments of the loop of Henle and collecting duct; urea is present in the interstitium ONLY in the inner medulla when it recycles from inner medullary collecting duct lumen back to the loop of Henle lumen.

Countercurrent Exchange in the Vasa Recta

Very little volume enters the medulla to be reabsorbed into the vasa recta, minimizing possible dilution of the medullary osmotic gradient.


In the medulla, the vasa recta picks up water and helps equilibrating solutes within medullary interstitium. Both descending and ascending vasa rectae equilibrate their contents with each other by countercurrent exchange mechanism.

ADH hormone functions to:

1. Regulate the water permeability of the distal tubule and the collecting duct.


2. Regulate the sodium transport across the proximal tubule epithelium.


3. Regulate the osmolality of the proximal tubule fluid.


4. Reduce the sodium transport across the collecting duct epithelium.


5. Increase the sodium transport across the descending limb of the loop of Henle.

Regulation of Renal Water Excretion: (regulation of ADH release)

Site for regulation of water balance is at the distal nephron (collecting ducts). The amount of water that is reabsorbed in the distal nephron varies with the amount of circulating ADH. No ADH= large urine volume; high ADH= small urine volume.

Source of ADH

ADH is synthesized in the hypothalamus and stored in the posterior pituitary until released.

Primary stimuli of ADH release

Plasma osmolality:


-Increases in plasma osmolality above a threshold value increases the amount of ADH released via stimulation of hypothalamic osmoreceptors. The opposite occurs when osmolality decreases when excess water is ingested.


-Increased plasma osmolality is the most potent stimulus for ADH release.

Secondary stimuli of ADH release

Blood Volume: secondary stimulus for ADH release. Increases in blood volume with resulting increases in BP inhibit ADH release via the action of the left atrial baroreceptors. Decreased blood volume results in disinhibition of this pathway, allowing more ADH to be released.

Sites of ADH action on water permeability:

late distal tubules and collecting ducts on the blood (peritubular) side.

Mechanism of ADH action:

Making the luminal membranes of distal nephron permeable to water through activation of adenylate cyclase which, by a sequence of events, finally results in the insertion of water channels into the luminal membrane.

Regulation of water intake.

Thirst mechanism is stimulated by the same stimuli that regulate the release of ADH (increased plasma osmolality, increased angiotension II as a result of decreased blood volume), but with less sensitivity than the ADH pathway. It is operated via the thirst center in the hypothalamus. The thirst mechanism complements the ADH regulation to maintain water balance (plasma osmolality).

Disorders of ADH system:

Diabetes insipidus: condition in which a person excretes LARGE amount of very DILUTE urine but otherwise normal. May be central (hypothalamus- no ADH) or nephrogenic (distal nephron not responding to ADH or no medullary gradient) in origin. The condition can be diagnosed by measurement of urine osmolality during water deprivation.