renal water balance

water input should =

water output

we output water through

urine, feces, sweat, exhaled air

water balance is maintained by

increased water intake

Bodies also get water from —- as a byproduct of cellular respiration

metabolism

control H₂O excretion independently of Na⁺, K⁺, urea – very important

kidneys

we aren’t aware that we are losing water, ex: We lose water when breathing

insensible loss

Kidneys will make the input and output of water

equal

is the least amount of water that the kidneys can produce in a day

500 mL

when talking about antidiuretic hormone we are referring to

arginine vasopressin

urine flow above usual levels

diuresis

low rate of water excretion (<0.5 ml/min) as hyperosmotic urine (really concentrated urine)

antidiuresis

normal urine flow =

1 mL/min

ALWAYS OPEN and Present in the Membranes of proximal tubules

AQP1

water permeable parts of the nephron in the absence of antidiuretic hormone

proximal tubule, thin descending limb of henle

water impermeable parts of the nephron in the absence of antidiuretic hormone

thick ascending limb of henle, distal tubule, collecting duct

water permeable parts of the nephron in the presence of antidiuretic hormone

proximal tubule, thin descending limb of henle, collecting duct

water impermeable parts of the nephron in the presence of antidiuretic hormone

thick ascending limb of henle, distal tubule

is the only segment that the water permeability changes, when antidiuretic is high, water is permeable - keeping water in the body, No antidiuretic hormone means it will be water impermeable and urine will continue to pass to the ureter to the bladder

collecting duct

urine - greater than 300, more concentrated

hyperosmotic

urine - less than 300, more dilute

hypoosmotic

Kidneys maintain plasma osmolarity at ——, countercurrent mechanism

300 mOsm

fluid in 1 tube flows in opposite direction to 2^nd tube, Greatly increases opportunity for exchange of H₂O & solutes

countercurrent flow

goes in opposite direction between cortex and medulla

tubule countercurrent flow

direction of blood flow in the medulla are countercurren

capillary countercurrent flow

requirement for production of concentrated urine through the countercurrent flow method for the loop of henle tubule and vasa recta capillary

hairpin loop

water leaving the tubular fluid, but sodium, K, Cl are staying in, requirement for concentrated urine in the countercurrent flow method

thin descending limb of the loop of henle

epithelial are impermeable to water, highly permeable to Na, K, Cl, requirement for the production of concentrated urine through the countercurrent flow method

thick ascending limb of the loop of henle

Descending & ascending segments, Both freely permeable to water & ions, passive exchange based on osmotic gradients and diffusion - requirement for concentrated urine production

vasa recta capillaries

Serves as osmotic equilibrating device, requirement for production of concentrated urine through countercurrent method

hypertonic medullary interstitium

ADH = AVP, ADH dependent water channels, AQP-2 (aquaporin), Passive reabsorption of water, requirement for production of concentrated urine through the countercurrent method

antidiuretic hormone

Generate hypertonic interstitial fluid in confined compartment in the renal medulla, Water permeable tube – collecting duct, Osmosis to drive water from tubule lumen

how to generate concentrated urine

Urine becomes dilute as moves through ascending limb loop due to Na⁺ reabsorption & H₂O —-

impermeability

the only aquaporins on the collecting duct

AQP3, 4

Vasopressin uses cAMP to cause AQP2 insertion into luminal membrane of principle cells of collecting ducts, Water flows out of tubular fluid of collecting ducts into renal capillaries, Urine can reach 1,200mOsm

concentrated urine

maximum concentration that urine can get to in humans

1200 mOsm

stimuli for ADH release: increased plasma osmolarity =

increased release of ADH

stimuli for ADH release: baroreceptors sense low pressure =

increase release of ADH

low pressure receptors for ADH are located in the

left atrium, large pulmonary

high pressure receptors for ADH release are located in the

aortic arch, carotid sinus

is the only protein in the kidney that is regulated by antidiuretic hormone, Will be increased in luminal membrane in response to increase antidiuretic hormone binding

AQP2

tubular action of ADH: AVP/ADH binds —- in the basolateral membrane of the collecting duct

V2 receptors

once AVP/ADH binds to the V2 receptors in the basolateral membrane of the collecting duct —— are inserted into the apical membrane to decrease dehydration by reabsorbing more water

AQP2

while water restriction means antidiuresis, severe sweating also means

antidiuresis

in relation to water to severe sweating, a high plasma concentration of ADH =

decreased water reabsorption

in relation to high water intake, low plasma ADH concentration =

decreased water reabsorption

severe sweating causes

decreased sodium and water excretion

most important stimulus for thirst under most physiological conditions

osmoreceptors

decreased plasma volume relayed to baroreceptors which cause angiotensin II to release which causes the feeling of

thirst

increased plasma osmolarity signals osmoreceptors which cause the feeling of

thirst

osmoreceptor pathway for severe sweating

increase plasma osmolarity, increase ADH, decrease water excretion

baroreceptor pathway for severe sweating

decreased plasma volume, increase ADH, decreased water excretion