Week 4 hypertension, control of BP Flashcards
what 3 factors stimulate renin release?
- reduced Na delivery to DCT- macula densa cells
- reduced perfusion pressure in the kidney- detected by baroreceptors in AA
- sympathetic stimulation to JGA- B1 adrenoreceptors noradrenaline
explain the RAAS system?
angiotensinogen made in liver- cleaved by renin to angiotensin 1- cleaved by ACE which is make by the lungs to angiotensin 2
this causes vasoconstriction including aff A of kidney, stimulates Na reabsorption at kidney so H2O follows and stimulates aldosterone from adrenal cortex which also stimulates Na reabsorption
how does angiotensin 2 affect kidney reabsorption of Na?
in PCT stimulates Na-H exchanger in apical membrane
how does aldosterone act to increase Na absorption in the kidney?
acts on principle cells of CD- stimulates Na and aquaporin channels so H2O reabsorption
- activates apical ENaC and apical K channels
- increases basolateral Na extrusion via Na/K ATPase
what affect does ACE have on bradykinin and why is that important?
ACE also breaks down bradykinin which is a vasodilator
taking ACE inhibitors will increase bradykinin and can result in a dry cough
how does the sympathetic NS control Na reabsorption in the kidneys?
vasoconstriction of arterioles= decreased GFR
activates Na/H exchanger and N/K ATPase
stimulates renin release for JG cells- noradrenaline
how does ADH increase reabsorption of Na?
- increased H2O reabsorption in distal nephron by aquaporin 2
- also acts on thick ascending limb- stimulates Na/K/Cl transporter and increase aquaporin channel
- also causes vasoconstriction
how do atrial natriuretic peptides (ANP) work and how are they released?
ANP synthesised in atrial myocytes and released in response to stretch of cells in atria due to high BP
ANP increases Na excretion and therefore H2O
if low BP- no stretch so low ANP
what are the actions of ANP?
-vasodilation of AA so increasing renal blood flow= >GFR
inhibits Na reabsorption
what do prostaglandins do to the kidneys and why is this important?
Kidneys produce prostaglandins which act locally= vasodilation= increased GFR and reduce Na reabsorption
- acts as a buffer to excessive vasoconstriction produced by SAS and RAAS helping to maintain renal blood flow and GFR
what do NSAIDS do to prostaglandins and why could this be dangerous?
inhibit pathway involved in formation of prostaglandins
- if administer NSAIDS when renal perfusion already compromised can further decrease GFR as no prostaglandin vasodilatory affect leading to acute renal failure
where is renin released from in the kidney?
granular cells of the juxtaglomerular apparatus
