tubular fucntion 2 Flashcards
describe the renin-angiotensin system
liver produce angiotensinogen
JGA produce renin - renin convert angiotensinogen to Ang1
angiotensin converting enzyme convert ang1 to ang2
ang2 -> aldosterone
where is ang2 produced
lung
ACE there because large endothelial surface
where is aldosterone produced
medulla of the adrenal cortex
effect of ang 2
vasoconstriction - increase Bp
increase Na uptake - increase water reabsorption - increase ECF - increase BP
effect of aldosterone
increase Na and water retention
what is aldosterone
steroid hormone
what stimulates the production of aldosterone
released in response to ang2
decrease in bp - baroreceptors
decreased osmolarity of the ultrafiltrate
action of aldosterone
increase Na reabsorption - control 35g/na a day
increased K secretion
increased H ion secretion
acts on principle cells of collecting duct
increae expression of apical Na channel
increasse formation of Na-K ATPase pumps
MECHANISM of aldosterone
diffuse into cells
bind to steroid hormone receptor in cytoplasm
heat shock proteins bound to receptor
they are released when aldosterone binds
aldosterone receptors dimerises
acts as a TF
things transcribed because of aldosterone
TF
regulatory proteins
transport machinery
regulatory proteins action
open Na channels on apical membranes
describe hypoaldosteronism
reabsorption of Na in distal nephron reduced
increased urinary loss
ECF vol falls and there is increased renin, ang2 and ADH
cause: low BP -> dizziness, salt craving, palpitations
describe hyperaldosteronism
reabsorption in the distal tubule increased
reduced urinary loss
ECF increase = hypertension
reduced renin, ang 2 and ADH
increased ANP and BNP
causes: high bp, muscle weakness, polyuria and thirst
how does hyperaldosteronism cause thirst and polyuria
high osmolarity
therefore thirsty to increase osmolarity
drink more
urinate more
Liddle’s syndrome
inherited disease of high BP mutation in aldosterone activated na channel always on always reabsorb too much na = water retention = hypertension
low pressure baroreceptors
heart - atria and RV
High pressure baroreceptors
vasculature system - pul vasculature, carotid sinus, aortic arch, JGA
after LV and before capillaries
action of low pressure system
response to low pressure: signal through afferent fibres to brainstem - sump activity -ADH
response to high pressure - atrial stretch - ANP, BNP
action of high pressure baroreceptors
only to low pressure
signal through afferent fibre to brainstem - sump activity -ADH
JGA cells - renin released
what stimulates ANP
made in RA
in response to atrial stretch
action of ANP
vasodilation
inhibit Na reabsorption in PCT and collecting ducts
inhibit renin and aldoseterone
reduce BP
concentrations of k
main intracellular ion
150mmol/l in
3-5mmol/l out
effect of K
extracellular
high - depolarise mem - AP - heart arrhythmia
low - heart arrhythmia
action regarding K after a meal
increase plasma K
tissue uptake stimulated by insulin, aldosterone and adrenaline
