RAAS Flashcards
What stimulates the release of renin from the JGA?
decreased afferent blood pressure
decreased tubular NaCl (urine)
What is the function of renin?
cleaves angiotensinogen into angiotensin I
What is the function of ACE?
converts Ang I to Ang II
What is the function of Ang II?
constricts the efferent arteriole to increase GFR
stimulates the release of aldosterone from adrenal
Where/how is angiotensinogen released?
continuously from the liver
Plasma levels of angiotensinogen are increased by what?
glucocorticoids thyroid hormone estrogen (pregnancy) Ang II inflammation insulin
_____ _______ reflects angiotensinogen levels and renin activity.
Blood pressure
Ang II is a potent vaso________.
vasoconstrictor
Ang II stimulates _____ release.
ADH
Ang II promotes Na _______ in the ________ tubule.
reabsorption
proximal
Ang II increases _________ synthesis and secretion.
aldosterone
Renin is secreted as _______.
prorenin
Pregnant women and diabetics have ________ levels of prorenin.
elevated
The newest hypertensive on the market is of what class?
renin inhibitor
What is the renin inhibitor agent?
Aliskiren
Aliskiren decreases plasma renin activity by __-__%
50 - 80%
Aliskiren ______ Ang I and Ang II levels.
decreases
Aliskiren decreases BP by __-__ mm Hg.
10-15
Aliskiren _____ plasma renin concentration.
increases
Aliskiren is dosed how often?
daily
What are the adverse effects of Aliskiren?
mild diarrhea
suppression of hematopoiesis
hyperkalemia
In what groups is Aliskiren contraindicated?
pregnancy
those who have experienced angioedema
ACE ______ bradykinin.
decreases
Bradykinin is a vaso______ that promotes ___ and ____ loss.
vasodilator
Na
water
Inhibition of ACE creates what effects?
decrease in Ang II
increase in bradykinin
vasodilation and diuresis
Where is ACE located?
on the luminal surface of the endothelial and kidney epithelial cells
ACE inhibitors ______ plasma renin levels.
increase
ACE inhibitors ______ plasma Ang I levels.
increase
ACE inhibitors ______ bradykinin degradation.
decrease
What are the 3 classes of ACE inhibitors?
sulfhydryls
dicarboxylates
phosphonates
Which ACE inhibitor(s) is(are) the most therapeutically effective?
none; they are all equal
What are the clinical uses of ACE inhibitors?
HTN CHF left ventricular dysfunction post MI diabetic and nondiabetic neuropathy
What are the major adverse effects of ACE inhibitors?
hypotension cough angioedema skin rash dysgeusia neutropenia hyperkalemia
In what groups are ACE inhibitors contraindicated?
pregnancy
bilateral renal stenosis
severe CHF
What is the ending for ACE inhibitors?
-pril
The affinity of ARBs is so much ______ than Ang II that it is essentially ________.
greater
insurmountable
ARBs are not effective in _______ HTN.
low-renin
What is the MOA of ARBs?
block the activity of Ang II on the Ang II receptor and thus decreasing aldosterone and ADH secretion
What are the therapeutic uses of ARBs?
HTN
heart failure
diabetic neuropathy
What are the adverse effects of ARBs?
not different than placebo
Combining ACE inhibitors with ARBs can lead to what?
hyperkalemia
kidney injury
What groups are ARBs contraindicated in?
pregnancy
careful use in renally compromised patients
What is the ending for ARBs?
-artan
What is Entresto?
A combination of ARB with sacubitril (a neprilysin inhibitor)
In what population is Entresto recommended?
heart failure
