Heart and circulatory system Flashcards
blood and its components
blood is a fluid connective tissue (4-5 L in humans)
- develop in red bone marrow of vertebrae, sternum, ribs, pelvis
- arise from stem cells that give rise to myeloid/lymphoid stem cells
plasma, (fluid matrix)
erythrocytes (rbc), leukocytes (wbc), platelets (blood cells)
plasma
fluid matrix blood is suspended in.
aqueous solution of plasma proteins, ions (Na+, K+, Ca2+, Cl-, HCO-), dissolved gases (O2CO2), glucose, amino acids, lipids, vitamins, hormones and gases (91% water)
albumins
plasma protein.
osmotic balance, pH,
transport: hormones, waste, drugs
globulins
plasma protein
transport: lipids (cholesterol), fat soluble vitamins (immunoglobulin, antibody)
fibrinogen
plasma protein involved in blood clotting
erthrocytes
- contain hemoglobin (transports O2 from lungs to body)
- no nucleus/organelles
- flexible: squeezes through capillaries
- life span: 4 months
leukocytes
- defend body against infecting pathogens
- eliminates dead/dying cells, debris (macrophages)
platelets
- cell fragments enclosed in plasma membrane
- trigger clotting: stick to collagen that is exposed when blood vessels are damaged, release factors to bring more platelets to the region, seal off damaged site
hematocrit/packed cell volume (PCV)/erythrocyte volume fraction (EVF)
volume percentage of RBCs in blood
45% for men 40% women
anemia low hematocrit
when spun in centrifuge:
top layer
plasma
leukocytes and platelets
packed cell volume/hematocrit = erythrocytes
bottom layer
cardiac muscle (mechanical properties)
- longer sarcomere length -> more tension -> more blood returns -> greater stretch -> stronger contraction
- normal heartbeats cardiac muscle isn’t at optimal length
- rate and strength of beating altered by autonomic and endocrine inputs
heart structure
4 chambered pump
- 2 atria at top
- 2 ventricles at bottom
AV valves between atria and ventricles (tricuspid and mitral/bicuspid valve)
SL valves between vent and aorta/pulmonary arteries (aortic/pulmonary)
blood is pumped into the
1. pulmonary circuit: oxygenates blood and returns
2. systemic circuit: takes oxygenated blood into body
superior vena cava blood vessels bring de-ox blood into right atrium (left + right atria fill at same time) when enough pressure is created, flow through tricuspid AV valve and start to fill ventricles. once enough pressure, go into aortic SL valve
valves
2 or 3 flaps
pressure opened/closed (no ATP)
advantage to having two circulation systems
2 pressures
if pulmonary pressure high, capillaries (which exchange oxygen with alveoli), can push fluid out into interstitial fluid by lungs -> pulmonary edema
systemic pressure always higher than pulmonary
pressure highest in arteries, then arterioles, capillaries, venules, veins
systemic circulation: high blood pressure in arteries, pulsatile
- doesn’t fall to 0 between heartbeats
- rise up, heart is contracting
- slope down, heart relaxing
design of transport systems
circulatory system are large tubes for bulk transport over distance
F(flow) = change in pressure/resistance
R = 8(length of tube) (fluid viscosity)/pi (inside radius of tube)^4
- when heart beats, higher pressure at one end (by ventricle)
basic heart beat/cardiac cycle
systole: ventricles contracting (110-140 mmHg) (atria fill with boood, pressure in atria low)
made up of:
a) isovolumetric ventricular contraction (AV, aortic and pulmonary valves closed)
b) ventricular ejection: blood flows out of ventricle (AV valve closed, aortic and pulmonary valves open)
diastole: ventricle relaxing (chambers filling, atria contracting) (60-90 mmHg)
made up of:
a) isovolumetric ventricular relaxation (AV, aortic and pulmonary valves closed)
b) ventricular filling (AV valve open)
1. blood flows into ventricle
2. atrial contraction
- blood moves bc of pressure differences
after load
systemic vascular resistance (SVR), amount of resistance heart must overcome to open aortic SL valve and push blood volume into systemic circulation
preload
LVEDP is amount of ventricular stretch at the end of diastole (loading up for the next squeeze)
stroke volume
amt of blood ejected per beat from left ventricle and measured in ml/beat
=EDV(vol blood in ventricle after filling phase)-ESV(blood left in ventricle after contraction)
increases proportionally with exercise intensity
untrained ind: 50-70ml/beat to 110-130ml/beat during intense p activity
cardiac output
amt of blood pumped by heart in 1 min (L/min) (rest: 5 L/min, intense p activity 20-40)
CO=SV x HR
amount of blood going out per beat and # of beats per min
how can you vary force of contraction/how much blood pumped out/SV
amt blood pumped out=amt returned=amt stretched=amt force of contraction
parasympathetic and sympathetic nerve fibers innervate the heart from csrdioregulatory center medulla oblonglata in brainstem
influence pumping action of heart by affecting both heart rate and stroke volume
frank starling mechanism
inc stretch = inc force
- optimal sarcomere length = max # of cross bridges that can form between myosin heads and actin thin filaments
types of receptors
metabotropic: ind linked with ion channels on plasma membrane through signal transduction mech (G proteins) work with ligands like neutrotrans
ionotropic: form an ion channel port
AChR in heart: M2
muscarinic receptor, slow HR down to normal sinus rhythm after actions of sympathetic system
(metabotropic, particularly responsive to muscarine)
parasympathetic effect on heart
para: vagus nerve innervates SA node (cluster cells in right atria that gen electrical impulses that initiate heart beat) = pacemaker, inhibitory effect
- neurons produce Acetylcholine (ACh) neutrotrans, binds to ligand gated channels on cardiac cell membrane, K+ leaves, hyperpolarizes cell (also dec permeability of Na+ and Ca++) takes longer to depolarize and cause action pot -> HR dec
muscarinic receptor, slow HR down to normal sinus rhythm after actions of sympathetic system
(metabotropic, particularly responsive to muscarine)
sympathetic
nerves from thoracic region of spinal cord project to heart as cardiac nerves
- innervate SA and AV nodes, coronary vessels and atrial and ventricular myocardium
- inc HR and force of contraction, greater contraction for same end diastolic volume (inc stroke volume)
also, epinephrine and norepinephrine (catecholamines) from adrenal medulla (endocrine gland that sits atop kidneys)
in total affect:
1. channels that bring calcuim into cell
2. channels that allow calcium to leave sarcoplasmic reticulum
3. calcium troponin interaction (heart contracts faster)
4. reuptake of calcium into sarc ret (heart relaxes faster)
catecholamines (adrenergic neurotransmitters)
amine derived from amino acid tyrosine, act as hormones or neurotransmitters
- bind to 2 diff classes of receptors; a and b adrenergic receptors
- neurons that secrete them are adrenergic neurons
- norepinephrine secreting neurons are noradrenergic
norepinephrine
from postganglionic sympathetic neurons (CNS-> preganglionic fiber -> ganglion: cluster of nerves -> post ganglionic fiber -> organ
- inc rate and degree of cardiac muscle depolarization, inc in frequency in AP and force and velocity of contraction
how?
is agonist (binds to) for cell surface B andregergic receptors, which cause G-protein mediated syn and accumulation of cAMP in cardiac cells, opens Ca2+ slow channels, inc cells ability to depolarize, helps open Na+ channels
epinephrine/adrenaline
hormone released from adrenal medulla
- derived from norepinephrine, similar in structure/has same effect on heart
nerve signals to adrenal gland activate conversion of stores of norepinephrine to epinephrine and cause release
- inc cardiac output and BGLs
neurogenic vs myogenic heart
(in some crustaceans) beat under control of nervous system
(all other animals)
- contractions initiated within heart
- nerves control rate
cardiac muscle cells
branched, connected to one another via intercalated discs (at Z line of sarcomere) that have gap junctions
autorythmic
heart stimulates itself to contract at regular intervals intervals
- pacemaker (excitable) cells in SA node generate APs
have specialized cell membrane that allows Na+, K+, and Ca+ to cross and trigger their electrical impulses
cardiac conduction system
cardiomyocytes (heart muscle cells) contract via depolarization and repolarization of cell membranes via movement of ions.
1. wave of excitation spreads from SA node through atria -> AV node (slower transmission here, everything else rapidly) -> bundle of His -> bundle branches -> Purkinje fibers -> ventricular heart muscle cells -> causes vent contraction
how is beat generated at SA node?
rise up to threshold:
1. permeability to K+ is declining (less K leaving)
2. funny channels open at low membrane potential let Na+ in
3. transient Ca2+ channels open bring Ca in (fast open and close for the rest of it) (T-type channel, initiate)
peak:
everything else lowers, long lasting Calcium channels open (L-type channel, sustain)
repolarization:
1. calcium channels close
2. inc permeability to K+ (leaves out)
3. funny channels pick up a little at very end
so symp effect: inc permeability to Na and Ca, dec to K
para: opposite
funny channels
mixed sodium potassium current
dual activation by voltage and cAMP
2 adaptive significances
no electrical connection between muscle cells of atria and ventricles (just connective tissue)
- want slow transmission because want time for things to fill, don’t want atria and ventricles to pump at same time
AP in cardiac muscle longer than AP in skeletal muscle
long refractory period (tetanus not possible)
no self re-excitation, rate set by pacemaker
excitation contraction coupling
AP spreads from plasma membrane to T tubules (lumen of T tubules is continuous with extracellular fluid)
skeletal muscle: opens Ca channels in Sarc Ret
cardiac: AP opens voltage gated Ca channels in T tubule membrane, diffuses through channels from extracellular fluid into cell
binds to Ca receptors in sarc ret, opens channels, results in large net diffuse of Ca from sarc ret into cytosol, binds troponin, etc -> contraction
EKG
P wave: depolarization from SA node 0.08 to 0.10 sec
flat region between P and QRS: impulse traveling within AV node and bundle of His, atria repolariszing but masked by QRS wave
PR interval (onset of P to beginning of QRS) represents time between onset of atrial depolarization and onset of ventricular depolarization
QRS: depolarization of ventricles (fast)
S-T: vent are completely depolarized (corresponds to plateau phase of vent APs)
T wave: vent repolarize
arterioles
arterioles (small branches of arteries) deliver blood to capillaries
constrict and dilate to regulate flow and pressure of blood into capillaries
capillaries
capillaries: exchange material with interstitial fluid
site of exchange
thinnest walls (single endothelial layer)
no smooth muscle, large surface area
variation in contraction of smooth muscles of arterioles and precapillary sphincters (band of smooth muscle that adjusts the blood flow into each capillary) controls blood flow through capillaries
slower blood flow than arteries and veins to maximize exchange
two mechanisms drive exchange of substances
1. diffusion along concentration gradients
2. bulk flow
structure:
2 endothelial cells make up wall
intercellular cleft and fused vesicle channels allow water soluble substances to diffuse
O2 and CO2 diffuse across membrane (hydrophobic)
pressure of blood (hydrostatic pressure) higher than pressure of interstitial fluid at arteriole end of capillary bed -> causes solutes + water to be forced out of capillaries by hydrostatic pressure
at venous end, net force is pulling fluid back into blood
tissue fluid circulates (dynamic equilibrium) so that tissues receive solutes from cap pores
arteries
carry blood away from heart
walls:
1. inner endothelial layer
2. middle smooth muscle layer
3. outer layer of elastic fibers (elastin, in connective tissue)
thick walled - withstand high pressure, large diameter, low resistance to flow, stretched when blood flows out from heart
even when heart relaxes, walls rebound and give blood extra push so that artery return to normal size and keep blood flowing (this is why pressure doesn’t drop to 0)
venules
collect blood from capillaries
veins
return blood to heart
act as blood reservoirs and conduits
one-way valves prevent blood from flowing backward
blood moves through veins in response to
1. contraction of smooth muscle in walls of veins
2. contraction of skeletal muscle surrounding veins
starling forces
whether fluid will move out of or into capillary, depends on
1. net filtration pressure: hydrostatic pressure of blood in the capillaries minus hydrostatic pressure of tissue fluid outside the capillaries
2. oncotic pressure
exchange of fluid between capillaries and tissues
concentrations of solutes are generally same in tissue (interstitial fluid) and plasma
- protein conc of plasma is greater than int fluid
colloid osmotic pressure is greater in the plasma than in the interstitial fluid
equation
fluid out-fluid in
(hydrostatic pressure in capillary+colloid osmotic pressure of interstitial fluid (should be 0))-(hydrostatic pressure of interstitial fluid-colloid osmotic pressure of blood plasma)
colloid osmotic pressure
osmotic pressure exerted by plasma proteins (albumin)
oncotic pressure
difference between colloid osmotic pressure in the plasma and interstitial fluid
lymphatic system
not all fluid from tissues can be reabsorbed into plasma
collects excess interstitial fluid (becomes lymph), transports it to lymph ducts that empty into veins
key component of immune system
extensive network of vessels
- made of lymph nodes, spleen, thymus, tonsils
remove viruses, bacteria, damaged cells and cellular debris from lymph and bloodstream, defend body against infection and cancer
maintaining blood flow and pressure
impacted by
1. cardiac output
2. degree of constriction of blood vessels
3. total blood volume
autonomic nervous system and endocrine system interact to coordinate mechanisms using
nitric oxide: major inducer of vasodilation
endothelin: peptide and major inducer of vasoconstriction
vessel control
local control: meets needs of particular tissue
ex. active hyperemia: response to increase in metabolism of tissue
O2 used faster, metabolites inc, arterioles dilating to achieve enough blood flow
flow autoregulation: response to drop in blood pressure
vessel wall not as stretched, smooth muscle around arteriole contracting less strongly, dilates, flow restored
extrinsic/central controls: needs of whole body (sympathetic nerves and plasma epinephrine on arterioles in skeletal muscles)
ex. fight or flight
epinephrine released, dilate vessels, more blood flow to vessels in skeletal muscle
2 primary features of gas exchange
- respiratory medium
- respiratory surface
- thin
- large surface area
-moist (in order to dissolve in water to move in and out of epithelial cells)
- human lungs invaginated to keep from drying out
- moisture is added to air in mouth/nasal passages
ventilation
flow of respiratory medium over external side of respiratory surface
perfusion
flow of blood/other body fluids on the internal side of respiratory surface
gas exchange
simple diffusion of molecules drives exchange of gases across resp surface (higher to lower regions of conc)
area of resp surface set total quantity of gases exchanged by diffusion
benefits to air breathing/having lungs
allow air to become saturated with water before reaches resp surface
- helps reduce water loss by evaporation
- inc surface area for gas exchange
lung ventilation (two types of breathing)
positive pressure (frog)
- air forced into lungs by muscle contractions
negative pressure (mammals)
- muscle contractions expand lungs, lowering air pressure inside
- air pulled into lungs
- air exhaled passively due to relaxation of diaphragm and external intercostal muscles, elastic recoil of lungs (pleural membranes)
- can forcefully exhale as well
mammalian resp system
- airways filter moisten and warm entering air
a. nose and mouth -> pharynx, larynx, trachea (non muscular tubes, rings of cartilage) -> two bronchi leading to lungs (have cilia (moves mat up throat) and mucus (trap debri/bacteria) secreting cells)-> bronchioles (contain smooth muscle cells can control diameter) -> alveoli surrounded by networks of blood capillaries - contractions of diaphragm and muscles between ribs ventilated lungs (lowers pressure of air in lungs and causes air to be pulled inwards)
- volume of inhaled/exhaled air varies
- centers that control breathing located in brain stem (pons and medulla like cardio)
- use negative pressure breathing
pleura
double layer of epithelial tissue that covers lungs
inner layer (visceral): attached to lung surface
outer layer (parietal): attached to surface of chest cavity
fluid filled space in between allows lungs to move without abrasion
elastic, recoil: stretching of lungs stores energy that can be released when expelling air
tidal volume
amt of air moved in and out of lungs during inhalation and exhalation ( at rest around 500ml)
vital capacity
total volume person can inhale and exhale breathing as deeply as possible (max male: 4800ml, female: 3400)
residual volume
air remaining in lungs after as much air as possible is exhaled (males: 1200ml females: 1000ml)
how does air flow
in response to differences in pressure
PV=nRT
R=nRT/V
- at constant T, pressure of a gas is inversely proportional to its volume
how breathing works
need a change in size of thorax (chest cavity)
1. negative pressure interpleural space keeps lungs in contact with chest wall
2. surface tension of pleural fluid also leads to close apposition of the lung surfaces with the chest wall
3. lungs are compliant (stretchy) and elastic (recoil)
inhalation: diaphragm contracts/moves down, rib cage expands, inc volume, dec pressure, draws air into lung
exhalation: diaphragm relaxes, moves up, rib cage gets smaller, dec in volume, inc in pressure, expel air
pressure changes during breathing
Ptp: transpulmonary pressure: diff in pressure between inside and outside of lungs (Palv-Pip) equal and opposite to elastic recoil pressure of the lung
Pip: pressure in pleural space
Patm: pressure in nose, mouth, airways
under physiological conditions :
Ptp always positive, Pip always negative, Palv moves from slightly positive to slightly negative
inspiration pressure changes
breathe in: chest wall expands (inc in volume), lowers Pip
Ptp becomes more pos as result and lungs expand
now as lungs expand and increase volume, Palm becomes less than Patm and air rushes in
between breaths (end of expiration) pressure changes
respiratory muscles relaxed, no air flow Palv-Patm=0 (equal to e/o)
lungs always hace air in them, positive Ptp
negative Pip “hold” lungs open and chest wall in
pressure changes mid cycle
at mid cycle (peak of breath in), net air flow is 0 bc chest wall is no longer expanding but hasn’t begun to contract, lung size not changing, epiglottis open to atmosphere
Pip has gone from -4 to -7 due to the expansion of the chest wall (inc in volume) at end of inspiration
exhalation pressure changes
resp muscles relax, chest wall and lungs get smaller due to elastic recoil
Palv inc, to above Patm
Pip returns to -4 value
lung compliance
measure of ease of expansion of lungs
2 determinants
1. stretchability of lunges (red by scar tissue)
2. surface tension: attractive forces between water molecules in the film of fluid that line alveoli
surfactant
surfactant: mixture of lipoprotein molecules in alveolar cells (type II pneumocytes)
- forms monolayer over surface of alveolar fluid/water molecules within alveoli that reduce the surface tension
- reduces cohesive forces between water m;olecules on alveolar surface, inc stretchability, prevent lungs from collapsing and forming smaller volume, fluid filled alveoli
control of breathing
control mechanisms
1. regulation centers in brain stem
2. local chemical controls
goal is to optimize gas exchange
match rate of air and blood flow in lungs
link rate and depth of breathing to body’s needs
rhythmical breathing
diaphragm and intercostal muscles are skeletal muscles
controlled by motor nerves whose destruction results in death
inspiration initiated by burst of APs in spinal motor nerves to inspiratory muscles, APs cease, ins muscles relax, expiration occurs as elastic lungs recoil
quiet breathing = little to no muscle contraction/relaxation involved in expiration (passive)
interneurons that regulate breathing
basic rhythm:
prod by neurons in medulla called medullary resp center
2 groups of neurons
DRG dorsal resp group: primaraly fire during inspiration, stimulates diaphragm.
have input to spinal motor neurons (phrenic (innervate diaphragm) and intercostal nerves)
VRG: adds to rate and depth of breathing by stimulating forceful exhalation and inhalation (excercise)
upper part of VRG (pacemaker cells + pre-botzinger complex) believed to compromise respiratory rhythm generator
blood gas control
medulla detects changes in levels of CO2 in blood and body fluids by receiving signals from peripheral chemoreceptors
1. carotid bodies
2. aortic bodies
central chemoreceptors (detect changes in CO2): located in medulla that send signals (excitatory synaptic input( to medullary neurons)
control centers in medulla and pons adjust rate and depth of breathing
stimuli for central and peripheral chemoreceptors
peripheral: respond to changes in arterial blood
1. dec Po2 (hypoxia)
2. inc H+ (metabolic acidosis)
3. inc PCO2 (resp acidosis)
central: respond to changes in brain extracellular fluid
1. inc in Pco2 via associated changes in H+ (can’t pick up H+ changes directly bc can’t cross blood brain barrier)
local controls in lungs
if air flow< capillary blood flow, O2 lvls in blood fall
smooth muscles in walls of lung arterioles contract, red blood flow, more time for blood to pick up O2
why is expired air fairly high in O2 content
- air flow is. way through bronchi and trachea. mixes fresh and used air bc we don’t expel all the air from the lungs each time we breathe
- air coming in includes some used air that was in dead space, not all air gets to the lungs
O2 transport
one hemoglobin molecule can combine with 4 O2
combines inside erythrocytes in heme group
O2 combined with hemoglobin maintain large partial pressure gradient between O2 in alveolar air and in blood
binding of O2 to Hb enhanced by cooperativity
in tissues:
less PO2 in tissues than blood
plus affinity of Hb for O2 is decreased by
- inc in CO2 (binds to hemoglobin and protons at a amino group and knocks O2 off)
- drop in pH (may come from inc CO2 or lactic acid
- inc in temp
(factors prod by active tissues)
it takes a drop of Partial pressure of O2 in arterial blood from 100 mmHg to 60 to hace saturation of hemoglobin start to drop
CO2 transfer
CO2 produced by cellular oxidation in active tissues, diffuses from cells to interstitial fluid to blood plasma
partial pressure of CO2 is higher in tissues than in blood
- 10% dissolves in plasma
- 70% converted to H+ and HCO-3 (bicarbonate) ions
- H+ combines with hemoglobin or proteins
- 20% combines with hemoglobin
in lungs:
partial pressure of CO2 higher in blood than in alveolar air
- CO2 released from blood into alveolar air
- rxns reversed to pack CO2 into blood
solute concentration
osmolarity in milliosmoles per liter mOsm/L
water moves osmotically from solution of lower osmolarity to higher osmolarity (from where there is more free water to where there is less)
hyposmotic = more water comparatively = hypotonic
osmotic pressure
min pressure needed to be applied to a solution to prevent the inward flow of water across a semipermeable membrane
diff approaches to osmoregulation
osmoregulators and osmoconformers
excretion is part of this
extracellular fluids filtered through tubules formed from transport epithelium (layer of cells with transport proteins in their membrane) and released as urine
what gets reabsorbed/secreted
glucose, amino acids, ions na k cl water, HCO3-
in kidney this occurs in proximal convoluted tubule
secreted: H+ and K+ maintaining ion and pH balance
in kidney, occurs mostly in distal convoluted tubule
excretion
getting rid of nitrogenous wastes
1. ammonia (aquatic animals), dilute
2. urea: ammonia with HCO3-, req less water (bc urine is hyper osmotic to body fluids)
3. uric acid: conserves more water
kidneys role in osmoreg
use is to conserve nutrients and water, balance salts, concentrate wastes for excretion
- nephrons have permeability differences (established by transport proteins in regions)
- diff concentration gradients of molecules and ions in interstitial fluid in kidney
- network of capillaries surrounding nephrons reabsorb ions, water, etc.
urine production
leaves individual nephrons -> processed further in collecting ducts -> pools in renal pelvis -> flows through ureter to urinary bladder -> urethra to exterior
blood flow in kidney
flows through renal artery -> interlobular artery -> afferent arteriole and enters glomerulus (cluster of blood vessels) in bowman’s capsule -> split into 50 capillaries that have very thin walls
- solutes filtered due to pressure gradient between blood and fluid in bowman’s capsule (controlled by contraction/dilation of arterioles)
after afferent arteriole, blood enters vasa recta (blood vessels near loop of henle
exits through renal vein
nephrons
specialized tubule
>1 million nephrons
juxtamedullary 20% long loops extend to medulla
cortical 80%: short loops mostly located in cortex
vasa recta
blood vessels around loop of henle in medulla region (peritubular capillaries located more cortically)
- imp in maintaining ion gradient of medulla to facilitate osmosis with loop of henle
processes involved in producing urine
- filtration (ultrafiltration)
bowman’s capsule (pressure driven)
- diameter of afferent arteriole and glomerular capillaries are relatively large
- efferent arterioles: receive blood from glomerulus has smaller diameter -> blood “backs up “ in glomerulus, keeping pressure high
- 47.5 gal of fluid each day
- high pressure forced small moleculares through the filter into glomerular capsule cans the basement membrane of Bowman’s capsule and into nephron
- fluid formed this way is called glomerular filtrate - reabsorption
- proximal tubule secretes H+ into filtrate, reabsorbs Na Cl K and HCO water and nutrients,
- Na+/H+ exchangers and Na+/K+ pumps in epithelium of tubule move Na from filtrate to interstitial fluid, results in voltage gradient which causes Cl ions to follow - secretion (N+ and NH3)
proximal tubule
reabsorpbtion of water ions and nutrients back into interstitial fluid main function
proximal tubule secretes H+ into filtrate, reabsorbs Na Cl K and HCO water and nutrients
Na+/H+ exchangers and Na+/K+ pumps in epithelium of tubule move Na from filtrate to interstitial fluid, results in voltage gradient which causes Cl ions to follow
- specific membrane proteins actively transport other things like glucose amino acids from filtrate in tubule to int fluid, filtrate now hypoismotic to interstitial fluid, water moves from tubule to int fluid via aquaporins
- all will move from int fluid to peritubular capillaries and return to the circulation
loop of henle
sets up gradient of solutes in interstitial fluid
- very high solute concentration towards pelvis of kidney
- descending segment has aquaporins for water reabsorption (can’t absorb salt though) (move out of tubule as it passes increasingly higher regions of solute concentrations of interstitial fluid in medulla) by bottom of tubule osmolarity of fluid in tubule = osmolarity of medulla fluid
- ascending is Na+ and Cl reabsorption
active transport, fluid in tubule has lower osmolarity as ascends towards cortex, no aquaporins - allows production of urine that is hyperosmotic to blood
counter current multiplier
design of loop of henle and vasa recta
- enables interstitial fluid in kidney cortex and medulla to maintain a concentration gradient
- helps keep blood coming from vasa recta to not be too hyperosmotic, allows water reabsorption, and production of conc urine
filtrate flow through LoH is opposite from vasa recta
ascending LOH releases Na which makes cell more solute
vasa recta capillaries have fenestrae (pores) that make them highly permeable to water and solutes, allowing for equilibrium. blood in vasa recta remains nearly isosmotic to interstitial fluid at each level so it doesn’t undo the osmotic gradient in the interstitial fluid
urea
highly soluble in water, practically non-toxic
cont to total osmolarity of interstitial fluid
diffuse into descending vasa recta. same solutes then diffuse out of ascending vasa recta then back into interstitial fluid
distal convoluted tubule
Na+, Cl HO and HCO3- are reabsorbed
K+ secreted and H+
collecting duct
- concentrates urine
- increasing solute gradient in the medulla
- some urea passively trans out of duct, adds to solute gradient in medulla
- H+ secreted into duct
renin
enzyme, a protease, also called angiotensinogenase
blood pressure regulation in kidney
water reabsorption in kidney can be regulated by ADH
- released from pituitary when osmoreceptors in hypothalamus detect an inc in osmolarity of body fluid
- angiotensin (peptide hormone) also stimulates secretion of ADH. inc water reabsorption, stimulates thirst
thirst review
- too little water in blood detected by hypothalamus
- more ADH produced by pituitary gland
- more water reabsorbed by kidneys, caused by ADH
- blood becomes less concentrated
negative feedback: hypothalamus detects change in blood concentration. pituitary produces less ADH, blood returns to correct osmotic concentration
sensors of blood pressure
- baroreceptors in aorta and carotids detect stretch and send signals to medulla oblongata in brainstem
- dec BP by activating parasympathetic nervous system and inhibitbition of sym - intra renal baroreceptors = juxtaglomerular cells -> renin (an enzyme) (leads to an inc in BP)
- Atria -> ANP (atrial netriuretic factor) protein hormone inhibits effects of renin and leads to BP dec
ANP promotes natriuresis (loss of sodium)
- atrial myocytes synthesize, store and release ANP in response to stretch
- cause renal vasodilation -> inc blood flow = inc glomerular filtration rate (GFR), more filtrate is processed, more urine (with Na+ and water is released
Na+ -> total fluid volume -> BP
kidney function - blood pressure
autoregulation system: involves interactions between glomerulus and nephron
filtration rate kept constant
juxtaglomerular apparatus: located in region where distal convoluted tubule contracts the afferent arteriole (which carries blood to glomerulus)
end result: signals from JG cells act to constrict or dilate afferent arterioles which keep blood flow and filtration constant
Renin- angiotensin aldosterone system (RAAS)
when blood volume and blood pressure drop, raise bP
renin (enzyme released from JGA) triggers angiotensin production by converting it to I which is converted to II (by ACE)
1. stimulates arteriole constriction
2. stimulates ADH (inc water reabsorption)
3. stimulants aldosterone (hormone from adrenal gland)
- inc Na + reabsorption
ANF inhibits fxs of renin
renin is protease (kidneys)
angiotensin hormone (liver)
aldosterone is hormone (adrenal cortex)
JGA
site of BP reg via RAAS in kidney
located side of glomerulus
formed by conjunction of cells of
1. macula densa (distal tubule)
2. juxtaglomerular cells of afferent arteriole
3. extra glomerular mesangial cells
macula densa
cells that monitor Na+ concentration in the filtrate and regulate via paracrine signals the release of renin by the adjacent JG cells
- low Na+ = macula densa cells signal JG cells to make renin
JG cells are specialized smooth muscle cells in the wall of the afferent arteriole which synthesize and secrete renin
- have beta adrenergic receptors (can induce secretion when stimulated by epinephrine)
sensor in atria -> ANP when bP is too high
actions of ANP opposite to renin
inhibits reabsorption of Na+ directly (on nephron)
inhibits release of aldosterone
ANP: causes dilation of afferent arteriole that leads to the kidney nephron while constricting the efferent arteriole
inc rate of blood flow into glomerulus
dec flow out of glomerulus via efferent arteriole
this increases GFR, inc prod urine, dec reabsorption of Na+ and water
renal acid base regulation
Na/H+ pumps in proximal tubule transport Na+ from filtrate into próx tubules and transport H+ from proximal tubule cells into filtrate -> combines with HCO3- to form H2CO3 carbonic acid. enzyme carbonic a hydrate CA located at apical cell membrane of prox tubule cell
converts HCO3 to H2O and CO2
in distal, H+ secreted into filtrate using H+ ATPase pumps (located on apical side) Na/K ATPase pumps located at basolateral membrane of tubule cells help maintain conc gradient which facilitates difff of NA+ into distal tubule cell
basic blood/too high PH alkalosis
less H+ present in filtrate to react with HCO30 in filtrate
result: less HCO3- reabsorbed, more in urine
acidic blood/pH too low
proximal tubule cells can make extra bicarbonate from metabolism of glutamine HCO3 is formed and released into the blood while ammonia (NH3) and ammonium ion (NH) are produced and enter the filtrate. The extra bicarbonate serves as a buffer in the blood. The ammonia (NHs) and the phosphates, HPO, - (which have been secreted into the filtrate) react with excess H+, allowing the H+ to be eliminated in the urine in a buffered state as NH and N2PO4
erythropoietin
EPO is hormone produced primery by kidneys
plays role in prod of RBCs
RAAS ORDER
renin angiotensinogen angiotensin I angiotensin II
