Renal: Sodium Flashcards
what is sodium necessary for
blood volume, pressure, organ perfusion
what are kidneys designed to do to sodium? why
designed to retain it because evolutionarily salt was scarce
normal sodium intake
rec 1600-2300, average 3500
how is sodium lost
sweat, diarhea, vomiting, hyperglycemia, diuretics
what do diuretics do
mess up kidney transport mechs, make you pee more, more sodium lost
how is sodium gained
diet, processed and fast food
how much filtrate is reabsorbed into the blood at each stage in the nephron
PT 70%, loop of henle 20-30%, distal 5-10%, cd 1-3%
when you have. sodium deficit how much gets excreted
less sodium gets excreted and more gets reabsorbed
what fluid volume is measured to monitor sodium balance
the plasma volume and ecf
where are sensors to sense sodium (3)
atrial baroreceps in carotid body and aortic arch, afferent arteiole in kidney, and atrial stretch receptor in the heart
what do aortic arch receps respond to
they register pressure in the aoorta, then signal vagus nerve x, then to brainstem
what do carotid sinus receps respond to
tehy register blood going to the brain, then signal sinus nerve, nerve ix, then brainstem
describe what happens when the baroreceps sense high vol blood
when they sense high blood volume, they have higher nerve signalling. through sensory nerve fibers they inhibit sympathetic outflow, and cause less heart activity
describe what happens when the baroreceps sense low vol blood
when there is low volume, they have lower nerve traffic, activate the symp system more, and increase cardiac output
when the sns is activated what does the renin angitenion system do
when the carotid is too empty, the sns gets activated. it secretes renin. renin converts angiotensinogen to ang , which uses ace to turn into ang 2. ang2 increases water and salt reabsorption (which will bring bp back up)
when the sns is inactivated what does the renin angitenion system do
this means that there was high wall pressure in ther carotid. so sns is inactivated, renin is not secreted. ang 2 is never made, thus cant reabsorb salt and water.
describe the renin angiotensin pathway
renin secreted, convers angiotensinogen to angiotension 1. angiotensin 1 gets converted to angitensin 2 by ace. ang 2 acts on the at1 receptor to increase salt and water reabsorption
how does the afferent arteriole respond to low pressures
afferent arteriole is in the kidney. if pressures fall, we want to raise bp. so renin is secreted, and RAAS pathway ensures, and water and salt reabsorption occurs
what does the macula densa have to do with low pressure in afferent arteriole
it senses arterial bp, and when there is low bp secretes renin
how does ang 2 impact NHE3
NHE3 is in the proximal tubule. if ang 2 has been made it means that we want to facilitate more salt and water reabs. so, ang 2 will stimulate nah exchange to bring more sodium into pt
how does ang 2 impact NCC
the ncc is in the distal convoluted tubule. its only responsible for reabsorbing 5-10% of the sodium. ang 2 will indirectly stimulate the ncc, and increase the na, cl reabs
where is NHE3
the proximal tubule
where is NCC
the distal convoluted tubule
what are the hemodynamic effects of ang 2
hemodynamic effects are actual alterations to the blood vessels. when ang 2 is released, it constricts the efferent arteriole.
what happens when ang 2 increases efferent resistance? why?
it lowers the hydrostatic pressure n the peritubular cap, but increases oncotic pressure, so it pulls water from the tubule
how is aldosterone made
ang 2 stimulates aldosterone release in the adrenal cortex. so, aldosterone is only gonna be made when ang 2 is made. and ang 2 is only made when we want to reabsorb salt and water…
what does aldosterone do in the collecting duct? what transporter does it impact?
we know the collecting duct is only responsible for reabsorbing 1-3% of the sodium. it increases the number of enac channels
describe the pathway of aldosterone in blood to reabs of sodium into blood
aldosterone combines with a cytoplasmic receptor
toegther, ald and receptor initiate nucleus transcription
translation and synthesis leads to new atp ase and new enac channels
proteins induced by aldosterons modulate the existing channels and pumps
you get more na in (to blood), more k in the lumen
what are the ways in which the sodium transfer of kidney is affected when you have no sodium, no water
no sodium no water, want to reabsorb both
the baroreceptors arent active, so sns is active. it stimulates the RAAS, producing ang 2
and 2 increases nhe, ncc activity, and contricts efferent arteriole, and generates aldosterone to impact enacs to increase na reabs
why does hot tub have same effect as high sodium
transmits pressure to interstit space, increases water in vasc compartment, baroreceptors expand. less ang 2, less na reabs (if you have excess sodium, you wouldnt want to excrete it)
what happens in the kidney when you have high sodium
when you have high sodium, you want to excrete more. therefore barorecep activation is increased, and RAAS shutdown. excess sodium also signals atrial stretch receps
where are the atrial stretch receps? what do they do
in the heart – in reponse to atrail stretch, myocytes secrete a hormone to reduce sodium reabs
how does more sodium activate atrial stretch receps?
higher vasc volume, higher stretch, higher ANP produced.
what does increase atria naturetic peptide do
reduces appetite (brain)
vasodilates to lower pressure (heart)
increases gfr and lowers na reabs (kidney)
whats the overall goal of activation of atrial stretch rceeps
when activated, reduce the reabs of sodium
how does anp affect collecting duct cells? what does it block?
joins onto the anp receptor, and makes cgmp
blocks enac, blocks na k atpase, blocks sodium symporters
does the body immediately respond to increased sodium?
