3.4.2. Vasodilator Drugs Flashcards
(68 cards)
1
Q
Purpose of vasodilators acting on arteries
A
arteries → reduce peripheral resistance (greater blood flow)
2
Q
Purpose of vasodilators acting on veins
A
veins → increase capacitance (larger volume stored in venous system)
3
Q
Purpose of vasodilators acting on coronary arteries
A
CORONARY arteries → improve cardiac blood flow
4
Q
Propranolol, Sotalol
A
β1 & β2-adrenoceptor antagonists = Propranolol, Sotalol
5
Q
metoprolol, Atenolol
A
β1-adrenoceptor selective antagonists = metoprolol, Atenolol,
6
Q
Labetalol, Carvedilol
A
α1- & β-adrenoceptor antagonists = Labetalol, Carvedilol
7
Q
Norepinephrine depletion drugs
A
Guanadrel, Reserpine
8
Q
α2A-adrenoceptor agonists
A
Clonidine, Guanabenz, Guanfacine
9
Q
fenoldopam
A
Dopamine D1 receptor agonists
10
Q
Drug types acting through autonomic nervous system
A
ACE inhibitors
ARBs (Angiotensin Receptor Blockers)
Aldosterone receptor antagonists
Renin inhibitors
11
Q
Captopril
A
ACE inhibitor
12
Q
Losartan
A
ARB
13
Q
Spironolactone and Eplerenone
A
Aldosterone receptor antagonists
14
Q
Aliskiren
A
Renin inhibitor
15
Q
MOA for Guanadrel
A
This is an exogenous false neurotransmitter that is accumulated, stored, and released like NE but is inactive at adrenergic receptors. Basically kicks out NE and takes its place.
- NET actively transports guanadrel into adrenergic neuronal storage vesicles.
- NE is displaced, resulting in specific inhibition of peripheral post-ganglionic adrenergic neurons
16
Q
Adverse effects for Guanadrel
A
- effector cells become supersensitive to NE during adrenergic neuron blockade. This response is similar to that produced by postganglionic sympathetic denervation.
17
Q
MOA for Reserpine
A
- binds tightly to adrenergic storage vesicles in central
and peripheral adrenergic neurons and remains bound for prolonged period of time - the vesicular catecholamine transporter that facilitates vesicular storage is inhibited
- thus, nerve endings
lose their capacity to concentrate and store NE and dopamine
18
Q
Adverse effects for reserpine
A
- sympathetic dysfunction and antihypertensive effects observed in reserpine-induced depletion of biogenic amines, so central and peripheral effects likely contribute to these effects
- Recovery of sympathetic function requires synthesis of new
storage vesicles, which takes days to weeks after discontinuation of the drug
19
Q
What are our Centrally-acting sympatholytic agents
A
Clonidine
Guanabenz
Guanfacine
20
Q
MOA for Centrally acting sympatholytic agents
A
- α2A adrenergic receptors in the brainstem are stimulated
- sympathetic outflow from the CNS is reduced
- plasma NE concentrations decrease (direct relationship w/sympathetic activity)
21
Q
Side effects for centrally acting sympatholytic agents
A
- at HIGHER doses, α2B receptors on vascular smooth muscle can be activated, inducing vasoconstriction
- loss of therapeutic effect observed at high doses
22
Q
What are the following drugs examples of?
Clonidine
Guanabenz
Guanfacine
A
Centrally-acting sympatholytic agents
23
Q
When do we use Hydralazine?
A
Clin Use: Severe HTN, CHF, HTN in pregnancy w/ methyldopa; frequently coadministered with B-blockers
24
Q
MOA for Hydralazine
A
Increase cGMP → smooth muscle relaxation; vasodilates arterioles more than veins; afterload reduction
It seems to prevent the development of nitrate tolerance, perhaps by inhibiting vascular superoxide production
25
Side Effects for Hydralazine
- reflex-related increases in HR
- cardiac contractility
- Lupus-like syndrome
- fluid retention
26
Hydralazine is contraindicated in who?
contraindicated in patients with both hypertension and coronary artery disease
27
MOA for Minoxidil
K+ channel OPENER
- metabolized to the active metabolite minoxidil sulfate that activates the ATP-modulated K+ channel
- channel opening causes hyperpolarization and relaxation (mainly in arteriolar smooth muscle, little effect on veins)
28
Side effects for Minoxidil
similar adverse effects to that of hydralazine
- also: plasma renin activity and fluid retention
- increases contractility and oxygen demand in the heart (can lead to cardiac ischemia)
29
Minoxadril is contraindicated in who?
contraindicated in hypertensive patients with coronary artery disease and patients with ventricular hypertrophy
30
MOA for Sodium nitroprusside
NO donor
- the “nitroso” functional group spontaneously and nonenzymatically releases a single NO molec
- vessel relaxation by NO is non-specific, so arteries and veins are BOTH affected
31
Side effects for sodium nitroprusside
- Excessive cyanide accumulation can lead to acid-base disturbances, cardiac arrhythmias, and even death
- Thiocyanate toxicity can also occur in patients with impaired renal function, causing disorientation, psychosis, muscle spasms, and convulsions
32
What are the following drugs an example of?
Sodium nitroprusside
Hydralazine
Minoxadril
Direct vasodilator drugs acting on vascular smooth muscle
| and/or the adjacent vascular endothelium
33
All Ca Channel blockers cause what
ALL Ca-C blockers:
| Reduction in contractility in vascular smooth muscle and the heart
34
Order of strength of vascular smooth muscle contraction by Ca Channel blockers
Vasc Smooth Muscle: amlodipine = nifedipine > diltiazem > verapamil
35
Order of strength of heart contraction by Ca Channel blockers
Heart: verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle)
36
Which Ca Channel blockers are dihydropyridine?
nifedipine, amlodipine,
nimodipine,
clevidipine
37
Which Ca Channel blockers are non dihydropyridine?
diltiazem, verapamil
38
General MOA for all Ca Channel blockers
- inhibition/blockage of L-type Ca channels (specifically binds to the alpha-1 subunit)
39
Effect of Ca Channel blockers in smooth muscle
- in SMOOTH MUSCLE: decreased Ca influx keeps intracellular [Ca] low
- Ca/CaM-mediated activation of myosin light chain kinase, actin-myosin
interaction, and smooth muscle contractility are all reduced
40
Effect of Ca Channel blockers in cardiac muscle
- in CARDIAC MUSCLE:
| decreased Ca influx decreases myocardial contractility, SA node pacemaker rate, and AV node conduction velocity
41
Effect of Ca Channel blockers in skeletal muscle?
- in SKELETAL MUSCLE:
| not significantly affected by Ca channel blockers b/c these cells depend on Ca release from the SR
42
Side Effects of dihydropyridine Ca Channel blockers
- Excessive vasodilation
| - depression of cardiac output
43
What do we use non dihydropyridine Ca Channel blockers for that we don't use dihydropyridine Ca Channel blockers for?
Atrial fibrillation/flutter
44
Side effects of nondihydropyridine Ca Channel blockers
- Excessive vasodilation
- depression of cardiac output
- AV nodal block
- potential precipitation of congestive heart failure
45
Verapamil is similar to ___ in effect
B blockers
46
____ is similar to nitrates in effect
nifedipine
47
This drug is contraindicated in patients with pheochromocytoma
Guanadrel is contraindicated in Pts with pheochromocytoma.
48
What is Theophylline?
Non-specific PDE inhibitor
49
MOA for PDE inhibitors
- prevent the hydrolysis of cyclic nucleotides (cAMP or cGMP) to their inactive monophosphate forms (AMP or GMP)
- increased cAMP causes positive inotropism in the heart, and dilation of both resistance and capacitance vessels in the peripheral vasculature
50
Which drugs are PDE 3 specific?
amrinone, milrinone, vesnarinone,
| dipyridamole
51
Which drugs are PDE 5 specific?
sildenafil, vardenafil, tadalefil
52
Where do we find PDE 3 specific PDE inhibitors
Cardiac and smooth muscle
53
Where do we find PDE 5 specific PDE inhibitors
Erectile smooth muscle.
Some amounts in retina and systemic vasculature
54
Side effects of all PDE inhibitors
- thrombocytopenia in about 10% of patients
| - severe side effects related to excessive vasodilation such as hypotension, MI, and sudden death can occur
55
Distinguish between oral and IV dose of Guandrel
When administered IV, an initial increase in arterial BP is seen because the sudden bolus causes a “surge” of NE displacement.. This response isn’t seen with oral administration because of a more gradual NE release; MAO has time to degrade NE as it is slowly displaced.
56
What is special about K+ channel openers?
Because K+ channel openers act by a mechanism that is entirely different from that of other vasodilators, these agents represent a potent family of drugs that can be used to treat hypertension refractory to other antihypertensive therapeutics
57
Use of Nitroprusside in the clinic
Used intravenously for potent hemodynamic control in hypertensive emergencies and severe cardiac failure. Because of its rapid onset of action, short duration of action, and high efficacy, sodium nitroprusside must be infused with continuous blood pressure monitoring and careful titration of drug dose to drug effect.
58
Which type of Ca Channel blocker is better at causing vasodilation?
Dihydropyridines.
Both do it, but DH are better than NonDH
59
Effect of Ca Channel blockers on AV conduction
Dihydro does not affect this
Nondihydros decrease the conduction
60
Effect of Ca Channel blockers on rate of recovery of the Ca channels
Dihydro does not affect this
Nondihydros decrease the rate of recovery
61
Effect of Ca Channel blockers on cardiac contractility
Dihydro increases HR by reflex
Nondihydros decrease contractility
62
Effect of Ca Channel blockers on HR
Dihydro increases HR by reflex
Nondihydros decrease HR dramatically
63
Drugs that we use for HTN EMERGENCIES
Nick can never find self HELP
```
Nicardipine
Clevidipine
Nitroglycerin
Fenoldopam
Sodium nitroprusside
Hydralazine
Esmolol
Labetalol
Phentolamine
```
64
Nicardipine vs. Clevidipine
Nicardipine has a long terminal half life
65
What emergency hypertensive is best for those with kidney issues
Fenoldopam
66
We use this emergency Hypertensive s/p CABG
Nitroglycerine
67
Our go to drug for aortic dissection
Esmolol
68
When we have HTN emergency in a pregnancy related eclampsia, we use this
Hydralazine
