Renal Lec 6 Flashcards
ADH/ vasopressin (type of hormone)
-peptide hormone (fast-acting)
osmoreceptors in …sense
hypothalamus sense increases in plasma osmolarity
ADH/vasopressin is produced by
cells of the SON of the hypothalamus
SON is in the
hypothalamus
SON stands for
supraoptic nucleus
vasopressin is stored in the
posterior pituitary gland
ADH secreted from
posterior pituitary gland
site of ADH action
collecting duct cells in kidney
mechanism of vasopressin action
alters water permeability of the luminal membrane of collecting duct cells
aquaporins (def.)
water channels found in renal tubule cells and other cells
number of aquaporins types in body
more than 10
type of aquaporins in proximal convoluted tubule
AQP1
type of aquaporins in collecting ducts
AQP2, AQP3, AQP4
ADH affects … insertion on… via
AQP2 insertion on the luminal side via regulation of AQP2 gene transcription
AQP on basolateral membrane
are not regulated by ADH (AQP3/4)
vasopressin receptors are on the (side of membrane)
basolateral membrane of tubule
vasopressin action mechanism (after attaching to receptors)
-vasopressin receptor activates adenylate cyclase which converts ATP to cAMP which activates PKA and causes a cycle of protein phosphorylation which control insertion of AQP2 in luminal membrane
in absence of ADH
- collecting ducts cells are almost impermeable to water
- extreme loss of large fluid volume (water diuresis)
ADH increased (pee less) by
shock, pain, warm, hot weather and water deprivation
ADH decreased (pee more) by
cold, humid environment, alcohol
diabetes insipidus
pathological condition: water diuresis, produce a large amount of dilute urine
central diabetes insipidus
failure to release ADH from posterior pituitary
nephrogenic diabetes insipidus
impaired renal tubule (especially in collecting ducts)
water diuresis (+pathological condition)
- only excess water is excreted without excess solute in urine
- diabetes insipidus
osmotic diuresis (+pathological condition)
- excess solute in urine is always associated with high levels of water excretion
- uncontrolled diabetes mellitus
relationship between body fluid volume & [Na+] regulation
-water reabsorption is dependent on Na+ reabsorption
plasma osmolarity mainly determined by
measuring the plasma Na+ concentration
changes in total body [Na+] cause changes in
blood volume and blood pressure `
low [Na+] in plasma- short term regulation
baroreceptors regulate GFR
low [Na+] in plasma- long term regulation
aldosterone promotes Na+ reabsorption (renin. angiotensin II needed for secretion)
high [Na+] in plasma- regulation
-atrial natriuretic peptide (ANP) regulates GFR and inhibits Na+ reabsorption and aldosterone
baroreceptors are (def.)
nerve endings that are sensitive to stretch
baroreceptors are located in
- carotid sinus
- aortic arch
- major veins
- intrarenal (JG cells of JGA)
baroreceptors sense
-changes in blood volume, peripheral resistance
baroreceptors (decrease in b.p causes)
-decrease in stretch, decrease in nerve impulse frequency, activation of (SYM branch) of the ANS, constriction of afferent arteriole, ↓GFR, ↓Na+ filtered , ↓Na+ exerted, ↑ Na+ in plasma
aldosterone (def.)
steroid hormone secreted from the adrenal cortex
aldosterone secretion triggered by
low sodium concentration
aldosterone effect is
long term
aldosterone (site of action)
-late distal tubule and cortical collecting duct
actions of aldosterone
- induces synthesis of Na+ transport protein
- stimulates Na+ reabsorption
- reduces Na+ excretion
Na+ reabsorption is linked to … secretion
K+
Na+ reabsorption (mechanism)
- Na+ diffuses into the CCD cell (luminal side), actively transported out of the cell via Na+/K+ ATPase (basolateral)
- K+ moves actively transported into the cell via Na+/K+ ATPase (basolateral) and diffuses into lumen via potassium channel
aldosterone affects which channels?
- Na+ channel on luminal side
- Na+/K+ ATPase on basolateral side
aldosterone regulation Na+ level
- low NaCL
- increased renin secretion
- increased plasma renin concentration
- increased plasma angiotensin I concentration
- increased plasma angiotensin II concentration
- increased aldosterone release
- increased aldosterone conc
- increased Na+ transporter synthesis/activity in CCD
- increased Na+ reabsorption
angiotensinogen secreted by
liver
renin produced by
juxtaglomerular cells of JGA in the kidney
renin is (def.)
an enzyme that helps control blood pressure
ACE stands for
Angiotensin-converting enzyme
ACE convertes
angiotension I to angiotension II
angiotensin cause
vasoconstriction and raise blood pressure
renin-angiotensin system (mechanism)
angiotensinogen –> (renin) angiotensin I –> (ACE) angiotensin II–> aldosterone (from adrenal cortex)
juxtaglomerular cells (location)
-on the wall of the afferent arteriole
juxtaglomerular cells are (type of receptors)
mechanoreceptors
juxtaglomerular cells sense
circulating plasma volume
low volume associated with
low sodium concentration
macula densa (location)
on wall the the distal convoluted tubule
macula densa are (type of receptors)
chemoreceptors
macula densa sense
NaCl load of the filtrate
renin conc. in plasma determined by
JG cells
- sympatheitc input from external barocrecptros
- intrarenal baroreceptors (JG cells)
- signals from macula densa
decreased stretch (low circulating volume)
renin release
increased stretch (high circulating volume) inhibits
renin release
renin angiotensin mechanism initiated in response to
- sympathetic stimulation of renal nerves
- decrease in filtrate osmolarity
- decreased blood pressure
the most important trigger for the release of aldosterone is
renin-angiotensin mechanism
what stimulates ANP secretion?
- increased NA+ concentration
- increased blood volume
- atrial distension (most important)
ANP is synthesized and secreted by
cardiac atria
site of ANP action
nephron (several tubular segments)
ANP action
- inhibits aldosterone actions
- inhibits Na+ reabsorption
- increases GFR and Na+ excretion
increase in cardiac atria distension leads to
↑ ANP secretion leads to =(all directly or via aldosterone)
-↓ plasma aldosterone, ↓ Na+reabsorption
-afferent dilation, efferent constriction = ↑ GFR
= ↑ Na+ excretion
K+ (renal handling)
- most filtered K+ is reabsorbed in proximal tubule + loop of henle
collecting duct can secrete
a small amount of K+
[K+] in urine is regulated in
CCD
hyperkalemia
excess K+ in blood
↑ extracellular {K+]
stimulation of aldosterone production
↑ [K+] excreted in urine
↓ extracellular {K+]
no aldosterone produced
↓ [K+] excreted in urine
