Renal II

ADH is produced in _ and released by _

supraoptic nucleus of hypothalamus ; posterior pituitary

ADH release by posterior pituitary is prompted by _

osmoreceptors in the hypothalamus

hypothalamic osmoreceptors stimulate (2)

H2O reabsorption from the urine

thirst center

ADH affects which parts of the kidneys

late distal tubule

collecting duct

how does ADH impact the late distal tubule/CD

increases permeability to water

ADH causes the production of _ urine

hypertonic

low/no ADH results in the production of _ urine

dilute urine

ADH does not alter the reabsorption of _

sodium

how does ADH increase water permeability

triggers incorporation of aquaporins into collecting duct membrane via vesicle fusion

aquaporin channels naturally reside in

membrane of intracellular vesicles within collecting duct

what happens to the collecting duct membrane without ADH

pinches inward to re-form intracellular vesicles

how does diabetes insipidus affect urine output

increased volume of urine output (ADH absent)

how does osmolality change as you move from renal cortex to medulla

increases

fluid leaving proximal tubule is _ to plasma

isosmotic

where does tubule fluid become hyperosmotic

descending limb of loop of Henle

what makes the medulla hyperosmotic

salt pumping from the ascending limb of loop of Henle

where does the tubule fluid become HYPO-osmotic

beginning of the distal tubule

what prompts the diffusion of water in the distal tubule/collecting duct

osmotic gradient due to the medulla being hyperosmotic

when does hypertonic dehydration occur

when a person loses water while retaining a high concentration of electrolytes/salts (more water than salt lost)

flow in opposite directions

countercurrent FLOW

countercurrent exchange is dependent on:

-countercurrent flow

-concentration gradient

countercurrent multiplier

a process that utilizes energy to create a concentration gradient

the interstitial fluid must be _ for H2O to be reabsorbed

hypertonic

which part of loop of henle is permeable to water

deescending loop

which part of loop of Henle has greater [Na]

ascending limb

how does Na enter the ascending loop of henle

Na/K/Cl cotransporter (2° active transport)

how does Na exit the ascending loop of henle

Na/K ATPase (active transport)

movement of Cl out of the ascending limb of henle

passively follows Na+ out

the vasa recta arises are specialized _ networks

peritubular capillary

vasa recta capillaries run _

parallel to loops of Henle of juxtamedullary nephrons

what impact do vasa recta capillaries have for countercurrent exchange

minimize washout of solutes from the medulla via recirculation

vasa recta _ medullary hyperosmolarity

maintains (does NOT create)

how does blood enter and leave the medulla

via vasa recta

vasa recta is permeable to _

solutes in the blood

plasma flowing down the descending limb of vasa recta becomes _

hyperosmotic

effect if the vasa recta wasn't U shaped

solutes would be lost from the medulla

ion/water movement in the descending vasa recta

water moves out

solutes diffuse in

ion/water movement in the ascending vasa recta

water moves in

solutes diffuse OUT

which parts of the kidney are permeable to urea

ascending limb of LH

terminal collecting duct

urea diffuses out of _ and into _

out: collecting duct

into: ascending limb of LH

vasa recta are associated with which kind of nephron

juxtamedullary

how does ADH affect urea absorption

increases permeability of urea in the collecting duct

collecting duct is impermeable to

NaCl

hormone responsible for homeostasis of plasma CONCENTRATION

ADH

hormone responsible for blood volume and BP

aldosterone

where does variability of Na reabsorption occur

distal tubules

collecting duct

what regulates Na reabsorption

aldosterone

where does aldosterone act on the kidneys

distal tubules

collecting duct

more Na is reabsorbed when _ is released

aldosterone

where does K+ secretion occur in the kidney

distal tubule

collecting duct

what impacts K+ secretion

intracellular K+

aldosterone

aldosterone impact on K+

increases K+ secretion and excretion

potassium is _ (what movements)

reabsorbed AND secreted

H+ can be secreted into renal tubules from _

peritubular capillaries

more H+ is secreted when _ is higher

CO2 concentration

renal tubules permeability to HCO3-

essentially impermeable

nephron cannot produce urine below pH of

4.5

secreted H+ must combine with _

buffers in the URINE

glomerular-tubular balance balances _

filtration with reabsorption

fluid volume excretion is affected by the same factors that affect _

GFR

reabsorption rate

increased plasma colloid osmotic pressure impact on excretion volume

decreases

5 factors that can impact volume excretion

1. tubular osmolar clearance

2. plasma colloid osmotic pressure

3. sympathetic stimulation

4. ADH

5. arterial pressure

how does increased arterial pressure lead to increased volume excretion

increases GFR

decreases reabsorption (high capillary resistance)

where is the JG apparatus found

where the afferent arteriole comes in contact with the thick ascending limb of LH

renin is secreted by _

granular cells within the afferent arteriole

K secretion =

K filtered + K secreted - K reabsorbed

renin converts _

angiotensinogen to angiotensin I

where is macula densa found

where the ascending limb is in contact with afferent arteriole

macula densa monitors _

[Na+]

decreased [NaCl] in macula densa causes:

dilation of afferent arteriole

increased renin release

angiotensin II has a greater effect on _

efferent arteriole

angiotensin II decreases _

renal blood flow

why does angiotensin II have a minimal impact on GFR

decreases renal blood flow while increasing glomerular pressure

angiotensin II impact on reabsorption

enhances

factors impacting renin release

1. plasma [Na+]

2. Cl- in tubular fluid of macula densa

3. stretch of JG cells

4. sympathetic stimulation

ANP is produced by

atrial cells

ANP effect on Na and H2O movement

promotes excretion

ANP is an endogenous _

diuretic

ANP effects

inhibits thirst

downregulates renin system

increases Na+ and H2O excretion

common causes of end stage kidney disease

diabetes mellitus

HTN

glomerulonephritis

causes of acute renal failure

decreased renal perfusion

obstruction

damage to kidney tissue

acute renal failure impact on creatinine

-increased blood [creatinine]

-decreased renal plasma clearance of cretainine

chronic kidney disease is often associated with what conditions

hypertension

diabetes

what happens to remaining nephrons in chronic kidney disease

irreversible sclerosis -> decline in GFR

what causes renovascular hypertension

constriction of renal arteries

effect of renovascular hypertension

triggers renin release due to decreased JG stretch (reduced blood flow mimics low BP signal)