Jackson 6 Flashcards by Tyler Brown

Two modes of transport

transcellular –

paracellular –

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transcellular –

molecules move through tubular cells

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paracellular –

molecules move between tubular cells

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osmosis – diffusion of water
solvent drag results from ——-

rate of water diffusion can be regulated by ——-

solutes being carried by water in paracellular transport

aquaporins

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endocytosis and exocytosis –

vesicular transport

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Sodium can be reabsorbed in all but one segment of a nephron - reabsorption occurs in the

proximal tubule, the ascending limbs of the loop of Henle, the distal tubule, and the collecting duct. The transport mechanism used varies.

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proximal tubule reabsorption–

Most of the reabsorption (65%) occurs in the

proximal tubule. In the latter part it is favoured by an electrochemical driving force, but initially it needs the cotransporter SGLT and the Na-H antiporter. Sodium passes along an electrochemical gradient (passive transport) from the lumen into the tubular cell, together with water and chloride which also diffuse passively. Water is reabsorbed to the same degree, resulting in the concentration in the end of the proximal tubule being the same as in the beginning. In other words, the reabsorption in the proximal tubule is isosmotic.

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thick ascending limb reabsoprtion–

Sodium is reabsorbed in the thick ascending limb of loop of Henle, by

Na-K-2Cl symporter and Na-H antiporter. It goes against its chemical driving force, but the high electrical driving force renders the overall electrochemical driving force positive anyway, availing some sodium to diffuse passively either the transcellular or paracellular way..

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distal tubule reabsoprtion –

In the distal convoluted tubule sodium is transported against an

electrochemical gradient by sodium-chloride symporters.

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collecting duct reabsorption -

The principal cells are the

sodium-transporting cells in the collecting duct system.

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Reabsorption in the proximal tubule

1. Glucose and amino acids are rebsorbed with

Na+ using symporters

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Reabsorption in the proximal tubule

Active transport on

basal side, keeps intracellular Na+ low

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Reabsorption in the proximal tubule

Water (and solutes) move via

paracellular transport; keeps the osmolarity of the tubular fluid constant

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Reabsorption in the proximal tubule

Na+ reabsorption also occurs in conjunction with

bicarbonate reabsorption using a Na+/H+ antiporter

reabsorption is not direct……H+ secretion = HCO3- reabsorption

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Reabsorption in the proximal tubule

CA reaction produces

H+ and HCO3- in tubule cell à HCO3- is transported into blood à H+ transported into tubular fluid where it recombines with a filtered HCO3-

Net effect is bicarbonate reabsorption

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The proximal tubule also has transporters for

organic cations and anions so such molecules are secreted into the tubular fluid. Many drugs are organic ionic compounds. They are commonly bound to plasma proteins so they are not filtered at the glomerulus, must be secreted in order for them to be excreted in the urine.

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Proximal tubule The transporters have low

specificity and can be saturated.

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To summarize: by the end of the proximal tubule –

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Reabsorption in the loop of Henle

In the loop of Henle,

25% of filtered NaCl and 15% of water is reabsorbed

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Descending thin limb -

impermeable to salt, but permeable to water

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Ascending thin limb -

impermeable to water, but permeable to salt.

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Reabsorption in thin limb segments is

passive

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In the ascending thick limb (ATL; see diagram at right), fluid is

diluted

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ATL: Na+ K+ 2Cl- symporter in

apical membrane

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ATL: Na+ K+ ATPase in

basolateral membrane

ATL: paracellular transport of monovalents and divalents NOT due to

solvent drag.

Tubular fluid becomes positive when

Cl- reabsorbed so cations diffuse along an electrical gradient

Fluid leaving loop is

hyposmotic, but the renal countercurrent mechanism has established an osmotic gradient required for formation of hyperosmotic urine.

Concentration of the tubular fluid will occur in the

collecting duct if antidiuretic hormone (ADH/vasopressin) is present.

The peritubular capillaries are permeable to

NaCl and water so plasma osmolarity changes as the capillaries follow the loop, but the osmolarity of the blood leaving the kidney (to veins) is normal.

Reabsorption in the distal tubule and collecting duct | The initial segment of the distal tubule, reabsorbs

~8% of filtered NaCl via a Na+ Cl- symporter in apical membrane and Na+ K+ ATPase in basolateral membrane

reabsorption of K+, H+ and water in distal tubule is

variable

Sodium reabsorption in the latter half of distal tubule and the collecting duct is

similar

There are two cell types in the collecting duct and late distal tubule

principal cells have epithelial sodium channels (ENaC) intercalated cells

epithelial sodium channels (ENaC) that reabsorb

Na+ and secrete K+

ENaC: | Na+ reabsorption drives

paracellular Cl- reabsorption

ENaC: | K+ secreted due to

Na+ K+ ATPase activity in basal membrane

intercalated cells involved with

acid-base balance; can also reabsorb K+

The activity of transport mechanisms can be modified to maintain

blood volume. A positive or negative shift in water balance shifts extracellular volume away from euvolemia (normal volume). Hormonal and neural responses to this shift help re-establish euvolemia

Hormonal regulation of blood volume -

ADH | Vasopressin or antidiuretic hormone (ADH) released from the posterior pituitary

Vasopressin or antidiuretic hormone (ADH) release is stimulated by high pressure baroreceptors in aortic arch and carotid sinus response to a decrease in blood pressure

changes in osmolality of body fluids

Vasopressin or antidiuretic hormone (ADH respond to osmolality above a set point of

275-290 mOsm/kg H2O

Vasopressin or antidiuretic hormone (ADH release can also be stimulated by

changes in blood volume/pressure

Vasopressin or antidiuretic hormone (ADH low pressure baroreceptors in

left atrium and large pulmonary vessels respond to a decrease in blood volume

Actions of ADH: | increases the permeability of the late distal tubule and the collecting duct to water by increasing

aquaporins into the apical membrane (basolateral membrane is freely permeable to water)

Actions of ADH | also increases permeability of

medullary collecting duct to urea

Actions of ADH If ADH low (diuresis) – solutes reabsorbed in

distal tubule and collecting duct, but no water reabsorption; urine as dilute as 50 mOsm/kg H2 O

Actions of ADH If ADH high (antidiuresis) – water reabsorbed as

fluid passes through collecting duct; urine can be concentrated up to 1200 mOsm/kg H2O

The renin-angiontensin-aldosterone system stimulates events that increase

reabsorption of sodium and water (combat volume contraction)

renin-angiontensin-aldosterone system: renin released in response to a drop in

perfusion pressure, decreased NaCl delivery to macula densa, or sympathetic input to juxtaglomerular cells

renin-angiontensin-aldosterone system renin converts

angiotensinogen to angiotensin I

renin-angiontensin-aldosterone system angiotensin I converted to

angiotensin II by angiotensin converting enzyme (ACE)

renin-angiontensin-aldosterone system angiotensin II has multiple effects

vasoconstriction stimulate release of ADH increase sympathetic activity stimulate aldosterone secretion

renin-angiontensin-aldosterone system aldosterone from the adrenal cortex acts to increase

NaCl reabsorption in the distal tubule and collecting duct by increasing transport protein synthesis

Natriuretic peptides are hormones secreted when the

heart dilates (during volume expansion)

Natriuretic peptides: | Atrial natriuretic peptide

from the atria

Natriuretic peptides | Brain natriuretic peptide from the

ventricles

Natriuretic peptides | The effects of natriuretic peptides include

vasodilation of afferent arterioles vasoconstriction of efferent arterioles inhibition of renin (and aldosterone) inhibition of ADH secretion

Natriuretic peptides Net effect is to increase the excretion of

NaCl and water.

Why is potassium regulation important? | K+ is a major determinant of

membrane resting potential. Therefore, it can affect electrically excitable cells.

Why is potassium regulation important? hyperkalemia will

depolarize Vm

Why is potassium regulation important? hypokalemia will

hyperpolarize Vm

Why is potassium regulation important? changes in K+ can cause

cardiac arrhythmias

How is potassium regulated? | ingested K+ is

fast shifted into cells – mediated by insulin, epinephrine, and aldosterone

kidneys typically excrete -------- of ingested K+

90-95%

Reabsorption and secretion of K+ in the nephron | In the glomerulus K+

is freely filtered.

In the proximal tubule about 67% of filtered K+ is

reabsorbed, mostly by paracellular transport / solvent drag as previously discussed for Na+.

In the thick ascending limb have reabsorption by

Na+K+2Cl- symporter and paracellular transport (non-solvent drag)

In the late distal tubule and collecting duct | K+ secreted by

principal cells depending on ATPase activity, K+ gradient, and/or apical K+ permeability or intercalated cells reabsorb K+ when potassium is depleted

Factors affecting excretion of potassium include plasma [K+] - increased K+ stimulates

aldosterone release, and aldosterone increases Na+ K+ ATPases in principal cells

Factors affecting excretion of potassium include flow rate of tubular fluid – increased flow rate increases

K+ secretion | local response to bending of cilia

Factors affecting excretion of potassium include ↑ flow --> ↑ ---- in collecting duct --> ↑Na+ ----- --> favors ↑ ----- secretion

Na+ reabsorption K+

Compare renal handling of potassium relative to plasma concentrations of potassium: Reabsorption in proximal tubule and thick ascending limb changes

very little

Compare renal handling of potassium relative to plasma concentrations of potassium Distal tubule and cortical collecting duct will

reabsorb potassium when plasma concentrations are low

Compare renal handling of potassium relative to plasma concentrations of potassium If plasma K+ is high, secretion

increases in distal tubule and cortical collecting duct