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BLOOD PRESSURE :revolving_hearts: AND RENAL SYSTEM :potable_water:…
BLOOD PRESSURE :revolving_hearts: AND RENAL SYSTEM :potable_water:
PROCESS
EXCRETION
establish osmotic gradient
VESA RECTA
permeable to
solute
water
COUNTER-CURRENT EXCHANGE
blood flows in a direction opposite the flow of tubular filtrate
protect osmotic gradient from being destroyed by water
scenario: active pumping of NaCl
decrease osmolarity in filtrate
increase osmolarity in interstitial fluid
water leaves passively in the descending loop of Henle
solute actively pumped out in the ascending LOH
CLEARANCE
inulin
glucose
urea
penicillin
CLEARANCE RATIO
appearance in urine
concentration of the substance
volume of the urine
appearance in the filtrate
concentration of the substance in the blood
draw some blood
GFR
a substance filtered through glmerulus
not reabsorbed
ratio
< 1 - more reabsorption
more than 1 - more secretion
Ex: inulin
penicillin even higher than inulin
= 1 - equal reabsorption and secretion
= 0 - reabsorbed all of the substance
Ex: glucose
FILTRATION
hydrostatic and colloid osmotic pressures
SCENARIO: glomerulus filtration rate
when dehydrated
increased colloid osmotic pressure
decrease GFR
MACULA DENSA
change GFR
directly: paracrine factors from macula densa
scenario: high NaCL in filtrate
signal: smooth muscle constriction of afferent arterioles
via ATP signaling
result: lower GFR
indirectly: renin- aagniotensin - aldosterone pathway
scenario: low NaCl in the filtrate
signal: muscle constriction of efferent arterioles
via renin- angiotensin - aldosterone pathway : juxtaflomerular cells
increase GFR
REABSORPTION
PROXIMAL CONVOLUTED TUBE
reabsorb
H2O : osmosis
glucose : secondary transports
tag along with Na thru SGLT
Na: Na/ K ATPase pump
Na channels: called ENaC
SCENARIO
ouabain
inhibit the Na/ K pump
decrease glucose reabsorption
decrease Na reabsorption
buildup Na inside the filtrate
ASCENDING LOOP OF HENLE
NKCC transporter
reabsorb 1 Na
reabsorb 1 K
reabsorb 2 Cl
establish concentration that exists in the renal medulla
transport max - point at which greater amount of a substance concentration cannot be used
SECRETION
why
some molecules are too big to be filtrated
still need to get rid of
examples
urea
peptidergic hormones
organic anions
ORGANIC ANIONS
NaDC
Na/ dicarboxylate transporter
pump Na from filtrate to proximal tubule
and pump Na & alpha KG in proximal tubule
OAT
alphaketogluterate out into interstitial fluid
anion in
some unknown transporter
organic ion in the filtrate - passive
A- in the proximal tubule cell
Na/ K pump
K into filtrate
Na out in interstitial fluid
BLOOD pH REGULATION
during acidosis
secrete H+
can't cross basolateral membrance
convert to CO2 to cross
reabsorb HCO3
K ride along with HCO3
during alkalosis
reabsorb H
secrete HCO3
K ride along with HCO3
notice transporter/ channels on the opposite sides of endothelial cells
REGULATION OF BLOOD PRESSURE
HORMONES
VASOPRESSIN
Scenario
no ADH :arrow_right: concentration of filtrate = osmolarity of the distal tubule
note: 'cause we don't actively pump water, so we need to establish a gradient concentration to move water across the membrane
the longer the loop of Henle the better the body is to reabsorb water
excess ADH = max concentration of the interstitial fluid / small volume
REGULATION
osmoreceptor
hypothalamus
osmolarity increase = more ADH
baroreceptors
aorta
carotid
low blood pressure = more ADH
detect pressure change
MODE OF ACTION
vasopressin bind to vasopressin receptor
=cAMP cascade = increase aquaporin on the collecting duct
= increase H2O permeability
= increase H2O reabsorption
increase blood pressure
lower osmolarity concentration
urea
ADH = increase permeability a urea transporter (UT-A1)
urea maintain the interstitial fluid osmolarity in case of water dilution
no ADH = still help maintain the osmolarity of the inner medulla
ALDOSTERONE
REGULATION
stimulated by
decrease blood pressure
RAAS pathway
activated by decrease of blood pressure
affect granular cells of afferent ateriole
produce renin
produce ANG I then ANG II
trigger adrenal cortex to produce aldosterone
increase K
inhibited by
very high osmolarity
MODE OF ACTION
reabsorb Na
create a greater gradient for H2O to move down the conc gradient
reabsorb H2O
need some ADH to reabsorb water
because aldosterone doesn't really reabsorb water
secrete K
elevated K lead to
cardia arrhythmia (pacemaker) and cardiac arrest (contractile cells)
convulsion (neuronal cells)
paralysis/ muscle weakness (skeletal muscle)
K in membrane potential
hyperpolarization of the membrane
location
distal tubule
early collecting duct
change in gene transcription
short-term
faster Na/K ATPase
longer opening times for Na and K
long-term
more pumps
new Na and K channels
ATRIAL NATRIURETIC PEPTIDE
MODE OF ACTION
inhibit
ADH release
aldosterone release
Na transporter in collecting ducts
reduce blood pressure
diameter
dilate afferent aterioles
constrict efferent arterioles
LOCATION
corin from the heart
BARORECEPTOR
how it works
= firing rate change in receptor carotid and aorta
= activate medulla
= change sympathetic : parasympathetic
pressure change
CHEMORECEPTOR
detect
low O2
low pH
increased CO2
how it works
after detection
reside in medulla oblongata
activate medulla
increased sympathetic tone
decrease parasympathetic
PRESSURE
RESISTANCE ELEMENTS
length of vessel
radius of vessel
viscosity of fluid
Poiseulle's equation
P = pressure
Q = flow
R = resistance
weird n = viscosity
pressure in cardiovascular
high in aorta
decrease when get to capillaries
so low in the veins
CAPILLARY EXCHANGE
forces
hydrostatic pressure
oncotic (osmotic pressure)
STARLING FORCES
net filtration = total (Pc + pi i) minus total (Pi + pi c)
permeability is a constant
lymphatic system
interstitial fluid flow into the
location
capillary
interstitial fluid
FILTRATION COEFFICIENT
