Cholinergic and Adrenergic drugs Flashcards
Phenoxybenzamine
Irreversible a1 and a2 blocker.
Useful for Renauds syndrome
Epinephrine
More potent at B2 than a1
Used for
- Bronchial asthma
- Anaphylactic shock
- Infiltration with local anesthetics for vasoconstriction to keep anesthetic local
Side effects: arrhythmias
Norepinephrine
Very weak at b2 receptors
IV infusion to maintain BP during spinal anesthesia or hypotensive shock
Isopropterenol
Potent at all b receptors, no alpha effects
Dopamine
Potent at D receptors
D1: Vasodilates renal BV, increases blood flow to the kidneys
D2: modulates NT release at nerve endings
Heart- mild increase in rate and force (partial agonist B1 and increases release of NE)
Blood vessels- high doses cause vasoconstriction and increased BP. In the situation of shock, this is an undesirable effect because decrease tissue perfusion
Dobutamine (Dobutrex)
B1 selective agonist
Clinical use: cardiogenic shock, MI, CHF
Adverse effects: may increase size of infarct.
Increases the work/O2 requirement
Phenylephrine
Non-catecholamine
A1 agonist prototype
Maintains BP in hypotensive states.
Nasal decongestant- vasoconstriction to decrease edema
- Vasoconstricition
- Increase peripheral resistance; increase BP
- Increased BP causes reflex bradycardia
Albuterol
Non-catechomamine
B2 agonist prototype (10x more potent at B2 than B1)
Main side effects: muscle tremors and tachycardia
Note: also salmeterol and formoterol- long acting bronchodilator for night time asthma
Amphetamines
Non-catechomamine
Indirect acting
Release NE from nerve terminals and inhibit NE reuptake by competition.
Crosses BBB
Used for: narcolepsy, AHDH, obesity
Pseudoephedrine
Mixed acting on alpha and beta.
Used for nasal decongestants
Access restricted. Used illegally to synthesize methamphetamine.
Phentolamine
Prototype reversible a1 and a2 blocker
Used for clonidine withdrawal
Prazosin
Selective a1 blocker
Generally reflex tachycardia is less prevalent than with non-selective alpha blockers
When 1st administered, may see syncope and orthostatic hypertension
Used for hypertension and BPH
Tamsulosin
Selective a1A blocker
Used for BPH
Propanolol
Nonselective beta blocker
decreases O2 demand and work on the heart (angina pectoralis)
Contraindicated in asthmatics and diabetics
- Blocks bronchodilation
- Masks signs of hypoglycemia
Is well absorbed following oral administration. Up to 75% may be inactivated by first pass metabolism.
Atenolol
B1 selective = cardioselective
Lessens risk of bronchospasm.
Metropolol
B1 selective= cardioselective
Lessens risk of bronchospasm but still contraindicated in asthmatics.
esmolol
B1 selective = cardioselective
Very rapid onset and short duration
Used as IV infusion for peri-operative tachycardia and hypertension
Labetalol
Selective a1 blocker
also a non selective beta blocker
- Partial agonist at B2
vasodilating
Carvediol
Nonselective B and a blocker
Lipid soluble and has antioxidant properties
vasodilating
Reduce mortality in CHF patients
Reserpine
Sympatholytic agent
Depletes NE by blocking vesicular transporter
Decreases CO but is a last choice drug
Clonidine
a2 agonist- sympatholytic agent
Activation of a2 in the brain decreases sympathetic outflow in the periphery and decreases sympathetic effects
Sudden withdrawal causes hypertensive crisis
Methyldopa
Sympatholytic agent
Compare with clonidine.
Acts like NE in disguise.
Stored in vesicles instead of NE. Released and acts a centrally acting a2 agonist.
Decreases central sympathetic outflow and decreases blood pressure
DOC for treating HTN in pregnant females.
“zosin”
a1 blocker
Pindolol
Beta blocker that is also a partial agonist
Carteolol
beta blocker that is also a partial agonist
Sotalol
Intrinsic sympathomimetic activity –> partial agonist
Clinical uses of beta blockers
- Hypertension: produces slow (weeks) decrease in peripheral resistance
- Ischemic heart disease
- MI and post-MI prophylaxis
- Congestive heart failure
- Arrhythmias
Thyrotoxicosis
Hyperthyroid pts have increased beta receptor sensitivity
Beta blockers reduces sensitivity of myocardium to adrenergic stimulation in hyperthyroid pts
beta blocker effect on exercise tolerance
beta blockers blunt the increase in HR and contractility that normally occurs with exercise
CO is less affected because stroke volume is increased
beta blockers decrease work capacity
increased catecholamines during exercise or stress increases the work of the heart and myocardial demand
Myocardial oxygen consumption
beta blockers decrease myocardial oxygen demand
Effects on plasma renin
Catecholamines stimulate B1 receptors in kidney juxtoglomerular apparatus to increase release of renin
- Beta blockers block this increase in renin
BP is decreased in most pts with elevated renin
betaxolol
B1 selective vasodilating beta blocker
sudden withdrawal of beta blockers
Rebound HTN
Anginal attack
Possibly MI
Beta receptor synthesis is increased by beta blocker use. Ex of receptor up-regulation, supersensitivity
a2 receptor agonists
centrally acting antihypertensive agents
- Control (inhibit) sympathetic outflow to periphery
- Decrease sympathetic tone
