-Similar to osmolarity but accounts for dissociative properties

-eg: 150mM of NaCl has 150mM of Na+ and 150mM of Cl-

TBW=60%

ICF=40%

ECF=20%

IF= 15%

Plasma= 5%

=#of particles/ Kg H20

*NOT dependent on temp b/c weight of water doesn't change with temp

T or F

If a membrane is permeable only to wate and two compartments seperated by this membrane initially contain different solute concentrations, when the compartments reach equilibrium the volumes of the compartments will be equal.

False. They will end at the same concentration of solute and water, but different volumes.

Solution that is more concentrated outside of the cell and causes the cell to shrink

Increased volume in ECF, but not changes in osmolarity therefore no change occurs in ICF.

1. Initially large increase in ECF volume and   osmolarity

2. Leads to water flow from the ICF to ECF

3. Leads to an increase in osmolarity of ICF

1. ECF volume increases --> decrease in ECF osmolarity

2. Water flow TO the ICF --> increase ICF volume

1. Find initial total osmolarity TBW(kg)*osmolarity

2. Subtract total excreted osmolarity=kg*osmolarity

3. Divide by change in body water (L)

ECF= Na+

ICF= K+

*The apex of a renal pyramid

*Leads to the minor calyx, then the major calyx, then the pelvis

*Major calyx and ureter/ urinary bladder

*Is technically an expanded portion of the ureter

Glomerular capillaries (thru visceral epithelia) -> bowman's space -> Promixal convoluted then straight tubules -> descending loop of Henle ->thin ascending LH -> thick ascending LH -> (macula densa) ->distal convulted tubule -> cortical collecting duct -> medullary collecting duct -> renal pelvis -> OUT

*Epithelial cells around the Bowman's capsule

*AKA visceral layer

*Blood vessels that run entire length of loop of Henle

*Only found in juxtamedullary nephrons

*Allow concentration of urine

-Renal corpsule is located in the cortex

-Has a short loop of Henle

-Lower filtration rates b/c nephrons are smaller

-No vasa recta

*Have vasa recta

*Long loops of Henle

*Located toward medulla and loops extend into medulla

Glomerulus

Bowman's space (both parietal and visceral layers)

*Glomerular capillaries contain fenestre

*Capillaries surrounded by basement membrane

*Photocytes of Bowman's capsule surround glomerular capillaries/BM and have slits that allow the filtration of water

*Slits= 40 Angstrom and have a negative charge

*Up to 20 A, free filtration

*20-42 A, filtration is variable

1. Macula densa: specialized cells that sense changes in [NaCl]

2. Granular (juxtaglomerular) cells: Produce Renin

3. Extraglomerular mesangial cells: SM like cells interspersed in extraglom space

1.Salt/ H2O regulation

2. Vit D regulation via Ca absorption/excretion

3. RBC production via erythropoietin in peritubular capillary endothelial cells

4. BP regulation

5. Excretion of xenobiotics (substances not normally found in the body, usually drugs, etc)

6. Excretion of metabolic waste

True or false

The proximal convuluted tubule lacks a brush border and mitochondria

False: the proximal convoluted tubule has a brush border to aid in reabsorption. It also has mitochondria

True or flase:

The ascending (thin and thick) loop on Henle has lots of mitochondria

False: they have few mitochondria

*Inulin clearance is used as a basis of comparision for clearance of other substances because is not secreted, reabsorbed, metabolized, or synthesized and is freely filtered

*Can be used to calculate GFR

*Blood vessels that travel alongside nephrons

*Allows reabsorption and secretion bwtn blood and lumen of nephron

*Rate of movement of fluids and solutes from glomerular capillaries into Bowman's space

GFR=Kf* (Hydrostatic glomerular capillary Pressure- hydrostatic Bowman's space pressure) - (osmotic pressure of glomerular capillary)

Glomerulas: Bowman's space hydrostatic pressure

 and oncotic pressure of glomerulus

Bowman's: GC hydrostatic, Bowman's oncotic

FF= GFR/RPF

RPF= (1-Hematocrit)* RBF

There are sharp decreases across the afferent and efferent arterioles

*Afferent arteriole resistance is changed to compensate for changes in BP

*Between a renal arterial pressure 80-160, GFR and renal blood flow remain constant

*Afferent arteriolar resistance is regulated by changes in flow rate in the tubule

*Change in arteriolar pressure -> change in glomerular pressure and plasma flow -> change in GFR -> change in Osm and NaCl whiched is sensed by macula densa, which sends signal to afferent arteriole --> changes in preglomerular resistance

*Regulates the tone of the afferent arteriole

*Tendency to contract when stretched

*Increased arteriolar pressure -> increased afferent arteriolar stretch -> increased contraction -> RBF and GFR are normalized

*If a substance is not metabolized or synthesized,

*Arterial input= Venous output + urine output

*Volume of plasma cleared of a specific substance  per unit time

*clearance= (urine[x]*urine flow rate)/Plasma[x]

*Initial decrease in excretion of creatinine, but it slowly increases back to normal

*No initial change in production of creatinine

* Increase in plasama [creatinine]

Between 99.2 and 99.9

Amino acids, protein, blood, ketones, leukocytes, and bilirubin

Na/Glucose transporter = cotransport

Na/H = countertransport

*Na+/AA

*Na+/H+

*Na+/Ca

*Cl/HCO3

*Na/H countertransporter

*Carbonic anhydrase on apical membrane converts bicarbonate into water and CO2

*In cell, water and CO2 are converted back to HCO3- by CA

*Na-K-Cl symporter drives into cell

*Leads to K secretion

*Na, Ca, K, and Mg cations can be reabsorped via paracellular transport

**Thick ascending LH is impermeable to water therefore it is called the diluting segment of the nephron

*Cotransport of Na/Cl

*Impermeable to water

-Na via ENaC channels

-K/H antiporter (K in, H out) in apical

-Carbonic Anhydrase in epithelial cell converts H2CO3 -> HCO3- and H+, HCO3- diffuses to IF, H into lumen

-H2O only reabsorbed if ADH present

-Late distal tubule/ collecting duct

-Diffusion of Na into the cell

-Inhibited by ameloride (Potassium sparing diuretic)

TF= concentration of substance or osmolarity in the proximal tubule fluid

P= blood plasma concentration

*Relative concentrations

*If proximal tubule reabsorbs 1/2 of water, and no inulin, the Tf/P value would double (because it is now twice as concentrated)

The IF is slightly/ "effectively" hypertonic because solutes are transported with a high affinity

Never: Thin and thick ascending loop of henl, distal convoluted tubule, and cortical tubule 

Only when ADH present: Cortical collecting duct and Inner-medullary collecting duct

Works in the proximal tubule by making the lumen/ fluid hypertonic -> less H2O reabsorption/ water remains in tubule -> excretion

Diamox is a diuretic used in the proximal tubule.

It inihbits the carbanic anhydrase -> eventual inhibition of flux -> more sodium in tubule -> increased excretion

Thiazides are duiretics that work in the distal convoluted tubule by inhibiting Cl- transport (which is coupled in cotransporter to Na+)

*work at TSC1

Furosemide and bumetanide work in the thick ascending limb. They compete for with the Cl- on the 2Cl/Na/K cotransporter (BSC1)

These are considered K wasting (b/c potassium is excreted) and are not used on patients with heart conditions.

-Works on the ENaC channel in the collecting duct.

-Inhibits Na reabsorption by binding to ENaC

-K sparing because it has little affect on K reabsorption

What is an example of something that is not filtered?Filtered, secreted and excreted? filtered and reabsorbed? Filtered and completely excreted (no reabsorption)?

1. Erythrocytes, proteins

2. Penicillin

3. Glucose

4. Creatinine

Na+

Cl-, HCO3-

*No change in proximal tubule because H2O/Na reabsorbed iso-osmotically

*Sharp increase in TF/P in the descending loop of Henle then sharp decrease in the ascending

*Past here it depends on conditions of diuresis or antidiuresis

 Antiduiresis: Osmolality increases a lot as water is

  reabsorbed and solute is not

 Diuresis: Osmolality decreases as some solute is

   reabsorbed and water is not

Anti: State of water conservation because of water restriction

Diuresis: Excess water -> excretion

Plasma osmolality and volume contraction

Increased ADH -> less water excreted -> increased urine osmolality

*Total solute excreted is constant, osmolality changes because of changing water amounts

Baroreceptors on coratid sinus, aortic arch, left atrium, and pulmonary vessels detect Vol/P change

-->

Stimulation of afferent vagus and glossopharnygeal nerves

-->

Input relayed to supraoptic and paraventricular nuclei

-->

Secretion of ADH

AVP binds V2 receptor ->

cAMP -> PKA ->
AQP2 insertion in apical membrane of epithelial cells

1. Fluid leaving proximal tubule is iso-osmotic

2. Water is passively reabsorbed in the thin descending loop, no solute reabsorption

3. NaCl absorption in thin/thick ascending but no water

4. Distal tubule and collecting ducts impermeable to water w/o ADH therefore

5. Medullary CD actively absorbs NaCl

Central: caused by trauma or pituitary surgery; decreased ADH production -> polyuria

Nephrogenic: Caused by mutations in V2 receptor or AQP2 gene; results in ADH resistance -> Polyuria

True or false:

When sodium intake is increased it leads to an increase in body weight because of a delay between intake and increased excretion

ΔIn blood Vol -> Δ in CO -> Δ in arterial pressure -> Δ in urinary output -> Δ in ECF vol -> Δ in blood vol

1. Vascular

    a. low pressure: cardiac atria & pulmonary vasc

    b. High pressure: carotid sinus, aortic arch,

       juxtaglomerular apparatus

2. CNS

3. Hepatic

*Autoregulation of renal plasma flow

*Tubuloglomerular feedback (increase GFR -> increased solute in macula densa -> decrease in resistance)

* Glomerulotubular balance

Increase GFR -> increased filtered load -> increased NA and H2O reabsorption by proximal tubules

*Glom sends signal to tubules to Δ

**constant fraction of Na/H2O is reabsorbed from proximal tubule despite Δs in GFR

↑ arterial pressure -> ↑ renal perfusion pressure -> ↑ medullary blood flow -> ↓ medullary tonicity -> ↑ renal interstitial hydrostatic pressure -> ↓H2O absorption from TDLH of juxtamedullary nephrons -> ↓ [Na] delivered to TALH -> ↓ Na retention -> ↑ Na excretion

1. Angiotensinogen is produced in the liver and is cleaved by renin (produced in the kidney)-->

2. Angiotensin I

3. Angiotensin I is converted to Angiotensin II

4. Angiotensin II acts in two places

    a. Leads to vasoconstriction

    b. Leads to production of aldosterone

        --> increased salt/ water retention

       --> increased BP

1. Increased angiotensin

2. Increased ECF

3. Increasd Systemic arterial pressure

4. Increased TPR/ vasoconstriction

5. Increased aldosterone

6. Increased Na retention

7. Increased GFR/ decreased proximal reabs. of Na

8. Change in sodium at macula densa

Renal

-Increase Na reabsorp in proximal tubules thru direct effect ( ) and through increased filtration fraction (via increased plasma oncotic P to favor reabsorption)

-Increase sensivity of tubuloglomerular feedback

-Decreased renin secretion

-Decrease medullary blood flow

Extrarenal

-Arteriolar vasoconstriction

-Increase aldosterone

-Increase ADH secretion

-Increase thirst

1. Increase in [angiotensin II]

2. Increase in plasma [K]

3.

Aldosterone binds receptor in cytosol -->

goes to nucleas --> change in gene expression

--> increase in expression/activity of ENaC and in Na/K ATPase

*Increased Na reabsorption

**Ramps up system

Latent pahse: 1/2 hr before response

Early phase: Increase in proteins that increase the activity of ENaC

Late phase: Increase in ENaC/ NaATPase  gene expression

1. Secreted in response to increase in blood pressure and ECF volume

2. Decreases blood pressure by decreasing TPR and enhancing NaCl and H2O secretion

3. Inhibits NaCl reabsorption by medullary portion of collecting duct

4. Inhibits ADH stimulated water reabsorption in collecting ducts

5. Inhibits ADH secretion from posterior pituitary