1/23
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
kidney functions
filtration, detoxification, cv homeostasis-water and salt retention
three endocrine signals
erythropoietin, cyp27b1, renin
what happens when too little and too much water is in the system
heart does not function properly, low blood pressure and o2. too much- pressure increases
too many substances in blood vs too little
tm- cells shrink, tl- cells burst
wasy to change solute concentration
can not just change volume. adjusted by removing na not water
glomerulus
capillary bed and has high pressure to push fluids into nephron
peritubular capillaries
capillary bed and low pressure
first part of the kideny tubule
water leaves by osmosis
2 part of kidney tubule
salt leaves by passive diffusion
3 part of kideny tubule
sakt pumped out
4-6 of kidney tubule
controlled concentration. if avp is present then its permeable to water and urea and if dehydtraded you reabsorb water
avp/adh
conserve water, increase volume, resistanec, and bp
ang2
conserve indirectly water increase volume, resistance, and bp, and reabsorb salt
aldosterone
conserve indirectly water, increase volume and bp, reabsorb salt
anp/anf
excrete water and salt, decrease volume resistance, and bp
vasopressin
increases water reabsorption
osmprecepter
detects sodium concentration plasma and changes cell size- more salt-receptor shrinks-signal release-adh
baroreceptor
in arteries and changes in vessel diameter to control vasopressin release
Central Diabetes Insipidus
lack of vasopressin secretion and is aquired, mutations. treated by vp therapy, hydration
nephrogenic diabetes insipidus
hereditary-recptor malfunction, treated by vp therapy, mild salt depletion
actions of angiostensin 2 in kidney
stimulates na uptake by kidney cells and na export from basal side of cell
what is aldersterone simulaed by
angiostin 2, is a steroid the binds to nuclear mr and stimulates sodium retention, k excretion
main drivers of aldosterone secretion
blood potassium and blood volume
aldosterone production
Triggered by the RAAS system (Renin-Angiotensin-Aldosterone System):
Low blood pressure, low sodium, or high potassium levels
Renin converts angiotensinogen → angiotensin I
Angiotensin I → angiotensin II (by ACE enzyme)
Angiotensin II tells the adrenal gland to release aldosterone