Lecture 2 Renal Flashcards
two modes of transport across tubular epithelial cells in a nephron are
transcellular and paracellular, what are these two?
transcellular- transport THROUGH tubular cells
paracellular- transport BETWEEN tubular cells
Osmosis results in solvent drag, what is solvent drag
solvent drag results from solutes being carried by water in paracellular transport
how can osmosis (rate of water diffusion) be regulated
by aquaporins
3 types of transported proteins and their definition
uniporter- 1 molecule moves
symporter (cotransport)- 2 molecules moved same direction
antiporter - 2 molecules moved in opposite directions (against concentration gradient)
endocytosis is what?
exocytosis is what?
endocytosis is transport into a cell
exocytosis is transport out of cell
BOTH BY Vesicles!
where is the ONLY spot in the nephron where Na is NOT reabsorbed?
Na NOT reabsorbed in the Thin Descending Limb of LoH
Na reabsorption %s in PCT? Thin ascending limb? thick ascending limb? DCT? Collecting duct
PCT-65% Thin AL: 7% Thick AL: 20% DCT: 5% Collecting duct: 2-3% SO KIDNEYS Excrete VERY LITTLE Na
The PCT reabsorbs several things
name them and how they are reabsorbed
Glucose, AAs= Na symporters
Active transport on basal side keeps Intracellular Na low
Water and solutes via paracellular transport
Na reabsorption in conjunction with Bicarbonate using Na/H antiporter
How is Na reabsorption done in PCT?
in conjunction with bicarbonate reabsorption using Na/ H antiporter
BUT reabsorption not direct H is secreted and HCO3 is absorbed
what rxn facilitates the absorption of bicarbonate
Carbonic Anhydrase produces H and HCO3 in tubule cells allowing HCO3 to be moved to blood and H is transported back into tubule so it recombines with filtered HCO3
LEADING To NET EFFECT of bicarbonate REABSORPTION
End of PCT what happens
2/3 of Na, Cl, and water reabsorbed and small proteins
K and divalent cations reabsorbed by solvent drag
AAs and glucose reabsorbed
Bicarbonate reabsorbed due to Na/ H antiporter
secretion of organic ions (IE organic drugs)
how much of filtered NaCl and water are reabsorbed in the LoH
NaCl= 25% reabsorbed Water= 15% reabsorbed
what is the permeability of salt and water in the the THIN Descending Limb
Thin DL= impermeable to SALT, Permeable to water
Bc it has aquaporins
permeability of salt and water in THIN ASCENDING LIMB
THIN ASCENDING LIMB
PERMEABLE to SALT (passive reabsorption)
IMpermeable to water
the ascending THICK limb has what to dilute fluid
Na K 2CL symporter in apical membrane
NaK ATPase in basolateral membrane
Paracellular transport of monovalent and divalents NOT DUE to Solvent Drag in THICK ascending limb
TRUE or FALSE
why?
TRUE! due to voltage gradient!!
Tubular fluid becomes positive due to Cl reabsorption so cations diffuse along an electrical gradient
fluid leaving LoH is hyposmotic then how do we get the formation of hyperosmotic urine?
renal countercurrent mechanism establishing an osmotic gradient allowing water to be reabsorbed in the collecting ducts by the actions of ADH (vasopressin)
In the absence of ADH what happens
no water reabsorption in collecting ducts so urine stays hyposmotic
how does the osmolarity of the blood leaving the kidneys to veins stay the same (normal)
bc peritubular capillaries are permeable to NaCL and water so plasma osmolarity changes as the capillaries follow the loop but returns to normal by the end
how does the DCT reabsorb about 8% of the filtered NaCl ?
VIA a Na Cy symporter in the apical membrane and a Na K ATPase in the basolateral membrane
describe reabsorption of K, H , and water in DCT
variable!
What 2 types of cells are in the latter DCT and the collecting duct?
Principal cells and Intercalated cells
what are principal cells in the late DCT and collecting duct for
Principal cells have ENaC channels that reabsorb Na and secrete K
Na reabsorption drives paracellular Cl absorption
K secreted due to Na K ATPase activity in basal membrane
What are intercalated cells involved in
Intercalated cells involved in acid base balance and help REABSORB K!
what is euvolemia
Euvolemia is normal blood volume
how is euvolemia maintained
hormonal and neural responses
What hormone is released by the Posterior Pituitary to regulate Blood Volume and what osmolality level does it responds to
ADH
release is stimulated by changes in osmolality of blood specifically to changes above a set osmolality of 275-290 mOsm/ kg of H2O
A dec in blood volume is sensed by what? (x2)
- low pressure barareceptors in LEFT atrium and large pulmonary vessels respond to DEC blood volume
- High pressure baroreceptors in AORTIC arch and CAROTID sinus respond to DEC in Blood Pressure (i.e. low Blood volume)
Actions of ADH?
ADH INC permeability of Late DISTAL tubule and Collecting duct to water by INC aquaporins into apical membrane
INC permeability of medullary collecting duct to urea
when is ADH released
when plasma level low or osmolality is HIGH
If ADH is low (diuresis) what happens?
ADH LOW = solutes reabsorbed in LATE DCT and collecting duct but NO water absorbed so URINE IS DILUTE and plentiful
what happens when ADH is high (antidiuresis)
ADH HIGH= water reabsorbed as fluid passes thru collecting duct and URINE IS CONCENTRATED up to 1200!
so urine excretion is low but concentrated!
ADH INC urea transporters thus causing reabsorption of water
renin - angiontensin- aldosterone system stimulates events that INC reabsorption of Na and H2O but how?
renin INC in response to DEC perfusion pressure and DEC NaCl delivery to Macula dense or SYMP input to JGA
renin converts angiotensinogen to angiontensin 1
angiontensin 1 converted to angiotensin 2 by ACE
what does Angiotensin 2 do?
Angiotensin 2 causes vasoconstriction, stimulate release of ADH, INC Symp activity, and INC aldosterone secretion
what does the release of aldosterone from the adrenal cortex do?
Aldosterone INC NaCl reabsorption in the DCT and collecting duct by INC transport protein synthesis
what are natriuretic peptides
hormones secreted when the heart dilates (during volume expansion)
atrial natriuretic peptides come from what
atria
brain natriuretic peptides come from what
THE VENTRICLES!
what are the effects of natriuretic peptides
VASODILATION of afferent arterioles ( INC GFR)
VasoCONSTRICT Efferent Arterioles (INC GFR)
inhibit renin and aldosterone
INHIBIT ADH secretion
NET Effect INC excretion of NaCl and Water
why is regulation of K important for Kidney
K is a major determinant of membrane resting potential therefore it can affect electrically excitable cells
what is hyperkalemia and result
INC K thus depolarizes Vm
what is hypokalemia and result
DEC K thus hyper polarizes Vm
what can changes in K cause
cardiac arrythmias
How is K regulated (x2)
Ingested K is fast shifted into cells by Insulin, E and Aldosterone
Kidney excretes 90-95% of ingested K
K if freely filtered in glomerulus so how much is reabsorbed in PCT and how
PCT reabsorbed 67^ of K thru solvent drag and paracellular transport
how is K reabsorbed in the Thick Ascending lim?
by Na K 2Cl simperer and paracellular transport (NOT SOLVENT DRAG!)
in the Late distal tubule and collecting duct what happens to K
K is secreted by principal cells depending on ATpase activity, K gradient and apical K permeability
or in cases of Low K intercalated cells reabsorb K
when body K is depleted what happens
Intercalated cells in late distal tubule and collecting ducts reabsorb K
If plasma K is INC what happens
INC K stimulates aldosterone release and aldosterone INC Na K ATPases in principal cells thus causing more K to be secreted
Inc Flow rate has what effect on K and why
INC flow rate = INC K secretion due to local response of bending of cilia and INC Flow favors INC Na reabsorption this favoring INC K secretion
when plasma concentrations of K are low what does DCT and cortical collecting duct do?
reabsorb K
if plasma K high what happens
DCT and collecting ducts INC secretion of K
