regulation of homeostasis by the kidney - fluid balance Flashcards
what does ADH do
CD impermeable to water but ADH can make it permeable
nonapeptide
vasopressin
half life 10-15 min
V2 receptors on basal membrane of principle cells in cd, inc camp = AP-2 water channels on apical surface
little conc urine
why is ADH released
in response to changes in plasma osmolarity and effective circulating volume
detected by osmoreceptors and baroreceptors
eg dehydration inc plasma osmolarity, ORs in hypothalamus, trigger ADH release to reabs more water and promote water intake
how does urea play a role in water reabsorption
freely filtered in g, reabs in PT but LOH/DT relatively impermeable to urea, urea can diffuse out of CD into medulla down conc gradient, adds to osmolarity of medullary interstitium
how is plasma osmolarity controlled
osmoreceptors in hypothalamus
ADH - kidney - excretion of water
thirst - brain - water intake
how is ECV controlled
baroreceptors (carotid sinus, aortic arch, renal afferent arteriole, atria of heart)
ADH, RAAS, ANP, SNS
short term - heart, BVs
long term - Na+ excretion
what are central vascular sensors
baroreceptors
low pressure blood vol receptors
important
large systemic veins, cardiac atria, pulmonary vasculature
what are high pressure arterial stretch receptors
less important baroreceptors
carotid sinus, aortic arch, renal afferent arteriole (the renal baroreceptor)
sensors also in CNS and liver - least important
how is ECV controlled
mediated by BR stim
changes in ECV trigger 4 parallel effector pathways which act on kidney
RAAS
SNS
ADH release
ANP release
change renal haemodynamics and Na transport by renal tubule cells
what is RAAS
renin (JGA) controls AngII
dec ECV stimulates renin release - dec renal perfusion pressure detected in afferent arteriole (renal baroreceptor)
dec Na conc in DT detected by macula dense cells (renal Na sensor)
brain BRs detects systemic BP drop to trigger SNS
effects of AngII
inc SNS tubular Na, Cl reabs and K sec, H20 retention aldosterone sec vasoconstriction CD H20 abs
what are the actions of AngII for
inc ECV
enhance Na transport in kidney
stimulation of aldosterone release from adrenal cortex
act on hypothalamus to stimulate thirst and ADH release into circulation
other effects of AngII
vasoconstriction on renal and other systemic vessels
longer term effects
renal cell hypertrophy (more protein synthesis of Na transporter and channels)
?role in hypertension
important actions of aldosterone
inc ECV
stimulates Na reabs (and K ex) in DT/CD
indirect neg FB on RAAS by inc ECV and lowering plasma K conc
important in conserving Na and water but also stopping K variation
what is Atrial Natriuretic peptide
lower ECV atrial myocytes synthesise and store it inc ECV = atrial stretch = ANP release promote natriuresis renal vasodilation - inc blood flow - inc GFR - Na excreted (MD, renin release reduced) inhibit renin and oppose AngII