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61 Cards in this Set
- Front
- Back
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What three things can peptides interact with
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-effector organs
-peripheral nervous system -central nervous system via circumventricular organs (leaky part of BBB that allows large peptides in) |
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What is the enzyme/molecule pathway for angiotensin?
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angiotensiongen (renin) --> AT I (converting enzyme) --> AT II (aminopeptidase) --> AT III (angiotensinases) --> peptide fragments
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T/F - AT I is active
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-false, only AT II and III are active
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What is the rate limiting factor in angiotensin production
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-amount of renin
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What 4 mechanisms control renin secretion
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-renal vascular receptor
-macula densa receptor -sympathetic nervous system -angiotensin II, VP, K+ (inhibit release) |
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How does the renal vascular receptor control renin release
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-senses a decrease in the stretch of the afferent arteriole which causes and increase in renin release
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How does the macular densa control renin release
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-senses a decrease in sodium and causes and increase in renin release
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How does the sympathetic nervous system control renin release
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-increase in renal nerve activity triggers NE release, binds to B-adrenoceptors in juxtaglomerular cells which causes increase in renin release
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What three molcules inhibit renin release
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AT II, vasopressin, K+
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Why do patients taking ACE inhibitors or AT1 receptor antagonists have increased renin and A1
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-because they lose AII feedback inhibition
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Patients taking ACEi or AT1 receptor antagonists have increases in what?
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-renin and A1
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Through what two ways does a decrease in arterial pressure cause renin release
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-renal baroreceptors (direct mechanism)
-systemic baroreceptors (indirect - uses NE on JG cells) |
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How does dehydration, hemorrhage cause renin release
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-decreases in blood volume are sensed by baroreceptors (SNS)
-increases in plasma osmolality are sense by osmolar receptors (SNS) |
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What three things stimulate renin release
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-decreased arterial pressure
-dehydration/hemorrhage -hyponatremia |
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What are the four actions of AT that cause an increase in arterial pressure?
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-direct vasoconstriction (AT1 receptors on smooth muscle)
-in CNS causes increased SNS and increased vasopressin -in PNS stimulates sympathetic transmission (NE) -in adrenal medulla stimulates release of epi |
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What are teh two cardiovascular effects unrelated to blood pressure?
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heart - increased rate and contractility (but is offset by baroreflex so no increase in BP)
hypertrophy - causes vascular smooth muscle cell growth |
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Dehydration results in what
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increased renin --> increased ATII which stimulates thirst and increases secretion of ACTH from pituitary
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T/F - ATII stimulates the synthesis and release of aldosterone
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true
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How does the renin/AT system have detrimental effects during CHF?
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-HF = decreased renal blood flow = increased renin = increased ATII = increased PR = increased afterload on heart, also increases water = increases preload on heart
-can cause hypertrophy due to direct and hemodynamic actions of AII |
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How does ATII promote sodium retention in the kidneys
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-vasoconstriction
-increased proximal tubular sodium reabsorption |
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How does ATII regulate is own production
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-feedback inhibition
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All angiotensin receptors are what kind of receptors?
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-GPCR
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What receptor mediates most actions of AII, AIII
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AT1
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What does the AT1 receptor stimulate and inhibit
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stimulates - PLC = increased Ca and PKC
inhibits = adenylyl cyclase, stimulates PLA2 |
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AT2 receptors:
-mediate what -effect on PLC/Ca signalin -how it works |
-vasodilation and natriuresis
-do NOT activate PLC or Ca signaling -opposes AT1 receptor mediated vasoconstriction |
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Which receptors are more common, AT1 or AT2
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-AT1 - therefore, vasoconstriction actions of ATII normally predominate
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AT2 receptors:
-mediate what -effect on PLC/Ca signalin -how it works |
-vasodilation and natriuresis
-do NOT activate PLC or Ca signaling -opposes AT1 receptor mediated vasoconstriction |
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T/F - AT3 mediates increased Ca
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-true
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AT2 receptors:
-mediate what -effect on PLC/Ca signalin -how it works |
-vasodilation and natriuresis
-do NOT activate PLC or Ca signaling -opposes AT1 receptor mediated vasoconstriction |
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Which receptors are more common, AT1 or AT2
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-AT1 - therefore, vasoconstriction actions of ATII normally predominate
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Losartan, valsartan, irbesartan, cardesartan are all
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-ARBs = angiotensin receptor blockers (competitive antagonists)
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ARBs:
-what they are -why are they better -what receptors they react to |
-potent nonpeptide AT1 antagonists
-lack some side effeects of ACEi -AT1 (10k-20k x more affinity than AT2) |
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T/F - AT3 mediates increased Ca
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-true
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Which receptors are more common, AT1 or AT2
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-AT1 - therefore, vasoconstriction actions of ATII normally predominate
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T/F - AT3 mediates increased Ca
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-true
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Losartan, valsartan, irbesartan, cardesartan are all
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-ARBs = angiotensin receptor blockers (competitive antagonists)
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Losartan, valsartan, irbesartan, cardesartan are all
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-ARBs = angiotensin receptor blockers (competitive antagonists)
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ARBs:
-what they are -why are they better -what receptors they react to |
-potent nonpeptide AT1 antagonists
-lack some side effeects of ACEi -AT1 (10k-20k x more affinity than AT2) |
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ARBs:
-what they are -why are they better -what receptors they react to |
-potent nonpeptide AT1 antagonists
-lack some side effeects of ACEi -AT1 (10k-20k x more affinity than AT2) |
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T/F - AT1 receptor antagonists affect kininase II
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-false
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T/F - the blood pressure-lowering effects of ARBs may be mediated in part by AT2 receptor activation
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-true
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Captopril, enalapril, lisinopril are all
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ACEi
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What are four uses of ACEi
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-antihypertensive (primary use)
-left ventricular systolic dysfunction -MI prophylaxis -heart failure |
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Side effects of ACEi
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-dry cough, hypotension, hyperkalemia, acute renal failure
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T/F - renin inhibitors are available for treatment of hypertension
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-false, still under development
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What effect do ACEi have in normotensive people
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-little effect because they have normal levels of renin
-only if the person was Na depelted - because they would have increased renin |
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How can ACEi be used to treat renal disease/obstruction
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-they promote hypertension via R/A system
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What two locations have a local R/A system where AT is formed and functions w/in tissues
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vascular smooth muscle - provides local intrinsic control
brain - functions as a NT, regulates SNS, AVP release |
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What three things cause ACP release
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-decreased arterial pressure (baroreceptor reflex)
-decreased fluid volume/increased plasma osmolality -pain, nausea, hypoxia, hormones |
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What three physiological actions does AVP have?
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-antidiuretic effect
-direct vasoconstriction (opposed by reflex bradycardia) -indirect central actions (area postrema --> vagal nuclei --> bradycardia) |
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What effects are V1 recfeptors responsible for
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-CV effects
-PLC increased = increased Ca -also PLA2, PLD activated |
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V2 receptors mediate what effects
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antidiuretic effects
-activated adenylyl cyclase = increased cAMP -mutations = cause one form of DI |
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Uses for:
V1 antagonists V2 antagonists |
v1 = HF, HTN, vascular disease
v2 = fluid retention assc w/ HF |
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How are kinins formed
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kallikreins act on kininogens
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What are the cardiovascular effects of bradykinin
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-vasodilator of arterioles via EDRF and eicosanoids = decreased Pa
-increase capillary permeability -stimulate sympathetic ganglia -stimulate EPI release |
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what would a kinin infusion cause in humans
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-decreased Pa
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What would a kinin antagonist infusion cause in humans
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-no effect unless pressor agent first administered (then would cause increased pressure)
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What types of vessels do kinins constrict
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-large arteries and most veins
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How do kinins relate to inflamation
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-produce edema, increase blood flow
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B2 receptor
-agonists -Mechanism |
-GPCR
-bradykinin and kallidin equally active -PLC, PLA2 |
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B1 receptor
-prefers --mediates |
-a different form of bradykinin
-contraction of vascular smooth muscle |
