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intrarenal RAAS system in CKD - Coggle Diagram
intrarenal RAAS system in CKD
renin release stimulated by: decrease in renal perfusion pressure , decrease in the delivery of salt to the macular densa and stim of sympathetic nerves via Bi adrenoreceptors
mice have 2 AT1 isoforms AT1A ans AT1B, AT1A is the murine homologue to ingle human AT1 recepor
tissue RAS
evidence
lack of markeldly elevated circ. renin or ANG II conc. in hypertensive disease states
ANG II conc. meausrued in renal tissues much higher than could be explained without circ ANG II
much higher conc. of AANG II in spec locations snd compartments of kidney indicated specific local reg of intrrenal ANG II
interstitial fluid and intratubular
kidney contains all the elements of RAS
ANGTOGEN produced by PCT which secrete it directly into tubule
ACE mainly associated to brush borders of PCT
Renin mRNA have been found in connecting tubule and CD
during periods of GM renin supression, upreg reninprod in DN may support continued intrarenal ANG II formation leadinfg to amplification or maintenace of hypertensive states
ROLE of intrarenal RAS in CKD
diabetic nephropathy caused by activation of IRAAS, causes CKD
diabetics prsent withvnormal or low PRA
howevee IRAAS seems to be activated as evidenced by
marked inc. in renal blood flowwith diabetes in response to an ACE inhibitor or ANG receptor blockade despite low p;asma renin activity
elivated urinary Agt
studies in PT AT1A KO in mice
GURLEY SB et al.
systolic BPs were sig lower in PTKO mice compared to baseline
vascular responses med by AT1 receptors not affected in the PTKO as response to acute infusion of VCs was identical in both groups
PRox fluid reabsoption is reduced in absence of PT AT1Ar
deletion of AT1AR from PT conveyed substantial protection against hypertension and sodium balence was also significantly reduced
mechanisms of dec BP and INC sodium exrection?
decreased expression of Na trnaporters in PT in PTKO