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44 Cards in this Set
- Front
- Back
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renin's funtion
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angiotensinogen --> angiotensin
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Rate limiting step of Ang II production
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Renin secretion
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Half life of Ang II
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30 seconds
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Three locations where complete RAAS have been found
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Heart
Vasculature Kidney generally cause hypertrophy and sclerosis |
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Ang II effects on hypothalamus
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stimulate thirst center
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Ang II effects on Posterior pituitary
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stimulate ADH secretion
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Ang II effect on GFR? RPF?
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GFR stays about the same
RPF goes down due to preferential constriction of efferents over afferents |
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Three causes of renin secretion
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Low perfusion pressure
Symathetic activity Low NaCl delivery to macula densa |
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ACEI
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Captopril
Lisinopril, enalapril, fosinopril ramipril |
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Captoril time of action
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Short
Taken 2-3x daily |
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Short acting ACE inhibitor
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Captopril
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Long acting ACE inhibitors
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Enalopril, lisinopril, fosinopril
ramipril |
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May be more effective because it is more lipophilic
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ramipril
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prodrug ACE I
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enalopril, fosinopril, ramipril
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Acitive drug ACE I
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captopril, lisinopril
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why captopril and lisinopril are different from other ACE I
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they are not prodrugs
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the difference between captopril and lisinopril
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captorpil is a short acting drugs (2-3x daily) and lisinopril is long acting (1/day)
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the two effects of ACE inhibitors
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block the production of Ang II
block the inactivation of bradykinnin |
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Main method of relief of CHF
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venodilation cause increased venous capacitance and lowers preload.
This bring heart back to more efficient contractile length and lower O2 consumption |
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these subgroups have low response rates to ACE I
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volume overload
salt-sensitive hypertensives blacks diabetics |
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exception to people with low response to ACE I subclass
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low-renin elderly still respond well
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how to get equivalent ACE I effect in blacks
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use with thiazides
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when will ARB work if ACE I fails?
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never
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Four uses of ACE I
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HTX
CHF Post MI (within 24 hours) Nephropathy (lowers BP that causes mesangial cell growth) |
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Advantage of ACEI over beta blocker
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Not contraindicated in asthma
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Advantage of ACEI over diurectics
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do not cause hypokalemia, hyperuricemia, hyperglycemia or hyperlipidemia
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Toxicities of ACE I
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hypotension
Renal failure (if already low RBF) hyperkalemia (if already low GFR) |
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Side effects of ACE I
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Cough
Birth defect in 2/3 trimester angioedema (mouth,tongue) |
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difference betwen AT1 and AT2 receptor
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AT1: hemodynamic and growth promoting effects of Ang II
AT2: apoptosis and tissues remodeling |
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When are AT2 receptors expressed
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fetal development and after arterial wall injury
always in the zona glomerulosa |
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Where are AT2 receptors contanstanly expressed
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Zona glomerulosa
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effect of AT1 block on renin
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Inhibits negative feedback so net increase in renin (and stimulation of ANT2)
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noncompetitive antagonist of ANT1
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Losartan
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competitive antagonist of ANT1
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Irbesartan
valsartan |
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Losartan
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noncompetitive antag of AT1
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Irebesartan
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competitive antag to AT1
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valsartan
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competitive antag of AT1
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when pregnant, this drug should be used for the RAAS
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none
both ACEI or ARB are contraindicated in pregnancy |
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advantage of ARB over ACEI
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ARB's (losartan, irbesartan, valsartan) do not cause cough and angioedema that ACEI do (captopril, lisinopril, enalopril, fosinopril, ramipril)
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location of production of ANP, BNP, CNP
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ANP: atria
BNP: atria CNP: CNS |
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Difference between BNP and other RAAS drugs
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increases GFR by relaxing afferents more than efferents and increases permeability
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synthetic BNP
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nesiritide
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nesiritide
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BNP analog, increases GFR and water excretion
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use of nesiritide
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acute cardiace failure by continuous iv administration
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