Osmoregulation by the kidney
Roles of Kidney
filters blood to remove wastes from body
osmoregulation (salt and water balance)
acid base balance
all of the above contributes to making urine
topics covered that the kidney is important for:
Ion concentration
need normal Na Cl concentrations in blood
too much Na+ outside makes the resting potential less than -70mV, it’s less ready to fire action potentials
hypoexcitable
hyperexcitable - more likely to fire action potentials, too little Na+
important to keep ions normal so action potentials can fire in heart and all over body
Blood pressure
kidney’s regulation of salt and water balance also affects blood pressure
too much H2O in blood increases blood pressure
too little H2O in blood/partially filled blood vessel leads to hypovolemic shock, which can cause a drop in blood pressure and reduced organ perfusion, potentially resulting in serious health complications.
Kidney
high O2 blood —>nephron —>ureter —> to bladder
processing of blood to make urine occurs at junction of cortex and medulla
nephron - renal tubule and blood vessels at the cortex and medulla junction
functional unit of the kidney
fluid flow through kidney’s nephron:
filtration, then reabsorption of nutrients, then reabsorption of salt and water
afferent arteriole —> glomerulus —> proximal renal tubule —> reabsorption or renal tubule —> loop of Henle —> distal renal tubule —> collecting duct
Afferent (inward) arteriole - delivers blood to nephron
Glomerulus - capillary modified for filtration
some blood bypasses for urine production and goes to afferent arteriole
Efferent (outward) arteriole - carries blood away from glomerulus
Renal tubule
glomerulus —> renal tubule
Bowman’s capsule (surrounds glomerulus)
Proximal tubule - closest to glomerulus
Renal tubule (Henle)
Distal tubule - goes down to
Collecting duct - now urine
4 processes of kidney:
filtration - potential to be urine
blood to renal tubule
glomerulus to Bowman’s capsule
~20% filtered; 80% efferent arteriole
reabsorption - in renal tubule to peritubular capillary
saved from urine
take good stuff aka nutrients and put in blood
H2O, suger, amino acids, etc.
secretion - blood to urine tubule
K+, H+
skipped filtration
excretion - urination
out of nephron
Filtration
~180L fluid filtered everyday
25% of blood supply when sleeping goes to kidneys
salt and water balance
too much H2O increases blood pressure
reabsorption - renal tubule back to blood
excretion - out of collecting duct = urine
out of nephron
end up with 1% of the 180L as urine
kidney functions:
remove wastes (afferent arteriole, glomerulus)
osmoregulation (loop of Henle, distal tubule, collecting duct)
Filtration at Glomerulus
plasma enters the afferent arteriole
80% goes to efferent arteriole, (away from glomerulus)
20% goes to glomerulus
filtrate goes to Bowman’s capsule then proximal convoluted tubule
The Glomerulus has pores
perforated
5nm pores
what is filtered?
plasma
made of water, ions, sugars
“plasma-proteins”
what is not filtered?
proteins (albumin, IgG)
cells: RBC, WBC, platelets
How fast does filtration occur?
adjusted by pressure
Glomerular Filtration Rate (GFR) is determined by Glomerular Filtration Pressure (GFP)
afferent arteriole vasoconstricts or vasodilates
glomerulus regulated by ANS
sympathetic - vasoconstrict
parasympathetic - vasodilate
PH = hydrostatic, blood pressure
~55 mmHg at capillaries
proteins remain in glomerulus
Pfluid = fluid pressure, push back from fluid already in Bowman’s capsule
π = osmotic pressure, higher osmolarity in glomerulus than in capsule
blood ~0.30 Osm = 300mOsm
include Na, sugar, Cl, amino acids, K, protein ions
everything dissolved added together
Osmolarity - all dissolved substances added together
glomerulus > capsule because proteins stay behind
if dehydrated, want filtration pressure to decrease, how?
reduce bp - vasoconstrict afferent arteriole
in this situation, sympathetic ns vasoconstricts
Macula densa - modified part of distal tubule
a flow meter, measuring flow rate
to loop of Henle
paracrine signal - chemical signal
tells afferent arterioles to constrict and slow down
begin production of urine
when flow was too high, now appropriate flow rate
Increase Autoregulation: kidney adjusts its own flow
autoregulation - any organ adjusting itself, digestive system good at it
more filtration, lose more urine
Reabsorption - renal lumen tubule back to blood
happens across transport epithelium
transport - fluid, molecules moving across a tissue
epithelia - sheet of cells making a barrier
epithelia transport
across one side of cell, through cell, then to other side, get through sheet of cells
epithelia
lined together by tight junctions so no gaps, form a sheet, not easily permeable
asymmetrical
blood side = basolateral membrane aka serosal side
apical membrane - full of microvilli to increase surface area
glucose reabsorption
pumped from renal tubule to blood
Secondary Active Transport
Na+ K+ pump always on basolateral side
3 Na+
2 K+ in
paired with K+ leak channel
Na+ concentration becomes low
Na/glucose co transport (diffusion)
energized by sodium gradient
strong gradient for Na+ powers this movement
GLUT
glucose channel - allows you to move down concentration gradient
facilitated diffusion
now glucose in blood is sent to muscles, insulin released
Secondary Active Transport
common in kidney and intestine
most water soluble nutrients use this mechanism
reabsorption mechanism for most water soluble nutrients (like glucose)
Filtration selectivity is only based on size
good and bad molecules
small toxins can also get filtered
Reabsorption - secondary active transport
selectivity for presence of co transporter (Na+ dependent)
makes sure nutrients needed are reabsorbed
things that get filtered out but not reabsorbed:
small enough to get through pores
no co transporters
gets urinated
Removal of wastes
filtered (nonselective) but not reabsorbed (selective)
smaller than 5nm but no co transporter
Osmoregulation - loop, distal tubule, collecting duct
Reabsorption in the proximal convoluted tubule is isotonic, and large magnitude (66% of filtrate)
66% of water filtrate reabsorbed in proximal convoluted tubule, 33% in loop/distal tubule/collecting duct
end of Proximal Tubule
large volume of H2O reabsorbed
no change in osmolarity - concentration of all soluble molecules added together
water pulled in by osmosis
isotonic
Reabsorption of solutes
Na+ reabsorbed by active transport
electrochemical gradient drives anion reabsorption
H2O moves by osmosis, following solute reabsorption
concentration of other solutes increases as fluid volume in lumen (tubule) decreases
permeable solutes are reabsorbed by diffusion through membrane transporters/paracellular pathway
Urine composition (water + Na+)
osmoregulation - salt and water balance
dehydrated - small volume and dark
concentrated urine (hypersomatic)
> 300 mOsm
overhydrated - large volume and clear
diluted urine (hyposomatic)
< 300 mOsm
300mOsm at end of Proximal tubule = no osmoregulation done
Water gain is mostly via drinking, and water loss is mostly via urine
lose some amount of water gained to maintain osmolarity
~1.5L water per day lost through urine
amount can be adjustable with hormones
Loop of Henle (renal loop)
Osmolarity of Extracellular fluid
in cortex isotonic (300mOsm)
gets higher further in renal loop
pull water out to make it more concentrated
4x more salty (1200mOsm)
then enough salt is pulled out to lower osmolarity
waste removal - proximal tubule
osmoregulation - loop, distal tubule
NaCl reabsorption - active transport
Thiazide
diuretics
increase urine volume
prescribed to lower bp
on ppt: b)
response to elevated bp & volume
increase blood volume
increase bp
kidney excretes salts (NaCl) and H2O in urine, decreasing blood volume & bp
thiazide diuretics block the Na/Cl co transporter of the distal convoluted tubule
more Na+ Cl- left in lumen to become urine
when co transporter blocked, H2O also blocked so diuretics take out water
increases urine output
“Loop diuretics” such as furosemide or bumetanide block the Na/2Cl/K symporter of the thick Ascending limb at the Cl- port
loop diuretics block cotransporter
Cl- Na+ H2O stays in filtrate
output as urine
diuretics slightly and chronically increase Na+, Cl-, H2O excretion
Collecting duct function w/out hormones
no hormones
impermeable to water
Anti diuretic hormone (vasopressin) increases water reabsorption in the renal collecting duct to make concentrated urine
makes less urine
absence of vasopressin increases bp
when release vasopressin increase water reabsorption
ADH - decreases urine volume
makes concentrated urine
>300mOsm
removing salts
dehydrated
water permeable
Vasopressin stimulates Aquaporin-2 movement from intracellular vescicles to the apical membrane
vasopressin/ADH
increase bp
increase water retention
vasopressin inserts water channels
aquaporin inserted into cell membrane, now cell membrane is permeable to H2O —> reabsorption of H2O
Regulation of blood pressure is acute, intermediary, and chronic - it is integrated across multiple organ systems
decrease blood volume —> drop in bp
decrease bp
so now,
kidneys increase blood volume
conserve salt & water to minimize blood volume loss
decrease urine output
Aldosterone is the “sodium saver” hormone, increase Na+ reabsorption in DCT
aldosterone acts on principal cells
aldosterone combines with cytoplasmic receptor
hormone-receptor complex initiates transcription in nucleus
translation and protein synthesis makes new protein channels and pumps
make new proteins
Na+ channels
K+ channels
aldosterone-induced proteins modulate existing channels and pumps
result in increased Na+ reabsorption and K+ secretion
Aldosterone and Atrial Natriuretic Peptide affect urinary Na+
aldosterone - sodium saver
increase NaCl retention
increase water retention
exchanged with K+ (pee out more K+)
aldosterone released when need to save salt (not take in enough)
Atrial Natriuretic Peptide is the sodium excreter
also acts on afferent arteriole, vasodilate
made in atria of heart
na-uretic = sodium rich urine
peptide - fast acting
blocks action of aldosterone
removes Na+ K+ channels
allows Na+ to travel out in urine
released when a lot of salt in body
decreases bp:
decreases Na+, NaCl excreted
H2O excreted
decreases blood volume
Hormones of salt and water balance
Aldosterone - sodium saver (increases Na+ reabsorption)
upper ascending loop & distal tubule
makes new Na+ channels (&K+ channels)
increase bp
Vasopressin/ADH - water retention/decrease urine volume
insert water channels (aquaporins)
increase water permability
collecting duct
increase bp
Atrial Natriuretic Peptide - sodium excreter
made in atria
opposite function to aldosterone
no low ADH -
increase water excretions
remove H2O channels
decrease bp
Changes im plasma volume and osmolarity
deviations from osmoregulation
pic on ppt
Hormonal responses to changes in plasma volume & NaCl
decrease plasma vol & increase osm - high ADH & aldosterone (Na+ saver)
increase plasma vol & increase osm - ANP(Na+ excreter) & low ADH
no change to H2O & decrease osm - aldosterone & normal ADH(don’t need to change vol)
Angiotensin II
the liver makes ANG and goes in plasma
renin converts ANG to ANG I
angiotensin converting enzyme ACE enzyme converts it to ANG II in plasma
ACE II converts ANGII to ANGI
low bp initiates afferent arteriole
acts on granular cells to make renin
next to macula densa are
granular cells - modified part of afferent arteriole
releases renin
aka juxtaglomerular (JG) cell
when low bp, renin is released
renin is NOT A HORMONE, it is an enzyme that makes the hormone
ANGII orchestrates increased bp
arterioles vasoconstrict
decrease vessel space
increase heart effort
hypothalamus increase vasopressin
ADH increases blood volume
hypothalamus increases thirst
adrenal cortex increases aldosterone
Covid infection
high bp
droplets breathed in lungs by COVID-19 spike protein, binds to ACE2 receptor in lungs
ACE2 decreases bp
eliminates ANG2 balance so a lot of ANG2 in COVID, high bp
Hyponatraemia Paper
thiazide induced hyponatraemia
increase urinary NaCl
increase urine volume
block NaCl cotransporter, more NaCl in urine
problems with elders taking thiazide:
hyponatraemia - low plasma Na+ concentration, normal plasma volume
resting potential goes up, hyperexcitability, neurons can fire quickly
hyponatraemia associated with
increased water intake, they drink more H2O
low ADH —> chronic hyponatraemia
patients - thiazide causes hyponatraemia
control - thiazide and no hyponatraemia
patients - low body weight, low plasma Na+ concentration before drug
Study design
baseline samples of blood and urine taken
one dose of drug, then samples are taken every 0,4,8,24 hours after
water & food intake were not regulated, patients drank more water
Table 2
patients w past history of hyponatraemia drink more H2O
b) both groups respond the same to the drug, baseline Na+ just lower in patients
c) difference occurs before & after drug
ADH normally released when dehydrated
patients drank more H2O so lower ADH
patients natrually drink more H2O and natrually have low blood sodium
may be dangerous
no cellular mechanisms differ in groups