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44 Cards in this Set

  • Front
  • Back
renin's funtion
angiotensinogen --> angiotensin

Rate limiting step of Ang II production
Renin secretion
Half life of Ang II
30 seconds
Three locations where complete RAAS have been found
Heart
Vasculature
Kidney

generally cause hypertrophy and sclerosis
Ang II effects on hypothalamus
stimulate thirst center
Ang II effects on Posterior pituitary
stimulate ADH secretion
Ang II effect on GFR? RPF?
GFR stays about the same
RPF goes down due to preferential constriction of efferents over afferents
Three causes of renin secretion
Low perfusion pressure
Symathetic activity
Low NaCl delivery to macula densa
ACEI
Captopril
Lisinopril, enalapril, fosinopril
ramipril
Captoril time of action
Short
Taken 2-3x daily
Short acting ACE inhibitor
Captopril
Long acting ACE inhibitors
Enalopril, lisinopril, fosinopril
ramipril
May be more effective because it is more lipophilic
ramipril
prodrug ACE I
enalopril, fosinopril, ramipril
Acitive drug ACE I
captopril, lisinopril
why captopril and lisinopril are different from other ACE I
they are not prodrugs
the difference between captopril and lisinopril
captorpil is a short acting drugs (2-3x daily) and lisinopril is long acting (1/day)
the two effects of ACE inhibitors
block the production of Ang II
block the inactivation of bradykinnin
Main method of relief of CHF
venodilation cause increased venous capacitance and lowers preload.
This bring heart back to more efficient contractile length and lower O2 consumption
these subgroups have low response rates to ACE I
volume overload
salt-sensitive hypertensives
blacks
diabetics
exception to people with low response to ACE I subclass
low-renin elderly still respond well
how to get equivalent ACE I effect in blacks
use with thiazides
when will ARB work if ACE I fails?
never
Four uses of ACE I
HTX
CHF
Post MI (within 24 hours)
Nephropathy (lowers BP that causes mesangial cell growth)
Advantage of ACEI over beta blocker
Not contraindicated in asthma
Advantage of ACEI over diurectics
do not cause hypokalemia, hyperuricemia, hyperglycemia or hyperlipidemia
Toxicities of ACE I
hypotension
Renal failure (if already low RBF)
hyperkalemia (if already low GFR)
Side effects of ACE I
Cough
Birth defect in 2/3 trimester
angioedema (mouth,tongue)
difference betwen AT1 and AT2 receptor
AT1: hemodynamic and growth promoting effects of Ang II

AT2: apoptosis and tissues remodeling
When are AT2 receptors expressed
fetal development and after arterial wall injury
always in the zona glomerulosa
Where are AT2 receptors contanstanly expressed
Zona glomerulosa
effect of AT1 block on renin
Inhibits negative feedback so net increase in renin (and stimulation of ANT2)
noncompetitive antagonist of ANT1
Losartan
competitive antagonist of ANT1
Irbesartan
valsartan
Losartan
noncompetitive antag of AT1
Irebesartan
competitive antag to AT1
valsartan
competitive antag of AT1
when pregnant, this drug should be used for the RAAS
none
both ACEI or ARB are contraindicated in pregnancy
advantage of ARB over ACEI
ARB's (losartan, irbesartan, valsartan) do not cause cough and angioedema that ACEI do (captopril, lisinopril, enalopril, fosinopril, ramipril)
location of production of ANP, BNP, CNP
ANP: atria
BNP: atria
CNP: CNS
Difference between BNP and other RAAS drugs
increases GFR by relaxing afferents more than efferents and increases permeability
synthetic BNP
nesiritide
nesiritide
BNP analog, increases GFR and water excretion
use of nesiritide
acute cardiace failure by continuous iv administration