Alpha 1 Agonists/antagonists Flashcards
Selective alpha 1 agonists
“-ine”‘
Aim to increase HR/BP
Vascular SM- vasoconstriction
Nasal Mucosa- vasoconstriction
Eye - vasoconstriction
Midodrine - shock / hypotension, orthostatic Hypotn
Phenyephrine, pseudoephedrine, oxymetaozline - nasal decongestant
Naphazoline = red eye drops
Selective alpha 1 antagonist
“-sin”
Least selective: Prazosin, Doxazosin, Terzosin
Vascular SM- vasodilation
Nasal mucosa - vasodilation
Most selective: Tamsulosin, alfuzosin, silodosin* (BPH)
Eye-vasodilation
Bladder- relaxation
ADRS: ED, abnormal ejaculation
Less selective: dizziness, syncope, hypotension, reflex tachy, first dose phenomena
Selective alpha 2 agonist
“-ines” pronounced eens - clonadine AND methyldopa (HTN in pregnancy)
Tizanidine, guanfacine, dexmedetomidine, bromododine, apraclonidine, clonidine
CNS - decrease stimulation
Sympathetic Autonomic NS - decrease release of NE/E
Eye - decrease aqueous humor (brimonidine, apraclonidine)
Clinical uses: HTN, ADHD, withdrawal, sedation, muscle spasms
Non selective alpha 2 antagonist
Ph “-amines”
Vasodilation while increasing CO
CNS- increase stimulation of SNS
Sympathetic autonomic NS - increase release of NE/E
Eye- increase aqueous humor
Clinical uses: male sexual dysfunction, psychosis
ADRS: nasal congestion, orthostatic hypotension
Selective beta 1 agonist
Dobutamine - IV - positive inotropic effects
SA node- increase sinus rate - bradycardia
AV node - increase AV nodal conduction - heart block, cardiac arrest
Atria/ventricle - increase FOC and SV - use AHF, cardiogenic shock, sepsis
Kidney- increase renin release (increase BP) - hypotn
ADRS: may lose selectivity at higher doses
Selective Beta 1 antagonist
-olol
Metropolol, atenolol, Nebviolol, bispropolol acebutolol, betxaolol, esmolol
* maintain selectivity at higher doses
SA node - decreease sinus rate - tachycardia, angina
AV node- decrease AV node conduction, arrhythmias
Atrial/ventricle- decrease FOC and SV - post MI, chronic HF, angina, arrhythmias
Kidney- decrease renin release (decrease BP) - HTN
Selective Beta 2 agonist
“-Erol” and terbutaline relax !!!! Vasodilation
SABA - albuterol and levalbuterol - asthma, COPD
LABA - all other -erols
Bronchial SM - bronchiodilation, relaxation
Uterine SM - relaxation - stop premature labor
Vascular SM - vasodilation
Skeletal muscle - increase glycogenolysis and tremors
Liver - glycolognlyisis and glucagenesis
Eye - increase aqueous humor production
Non selective beta 1 and 2 agonist
-enol
Isoproterenol
Beta 1 - stumiulatory, positive ionotropic - treat bradycardia and HTN
Metaproterenol
Beta 2 - dilation and relaxation - treat asthma and COPS
Non selective beta antagonists
-olol
Nadolol, propranolol, carteolol, Timolol, levobutanolol,metripranolol, solatolol (antiarrythmic), pinolol
Bronchial SM - constriction
Uterine SM - contraction
Vascular Sm- vasoconstriction - migraine prophylaxis
Skeletal muscle - decrease glycogenolysis and tremors- tremors, stage fright
Liver- decrease glycogenolysis and glucagenesis, decrease portal venous pressure - dec blood flow
Treat: portal HTN, esophageal vacancies, bleeding prophylaxis
Eye - decrease aqueous humor production - glaucoma, ocular HTN,
ADR: fatigue, masked signs of hypoglycemia, bronchoconstriction when pt taking B2 antagonist, servers peripheral vascular disease, heart blocks
Selective Beta 3 agonists
Mirabegron
Target: detrusor muscle in bladder
Effect: muscle relaxation - increase bladder capacity
Uses: overactive bladder, incontienance, urgency and frequency
ADRS: HTN, BP elevations, tachycardia
Why Beta 1 > Beta 2?
Mortality reduction in ACS, MI/M ischemia
Decrease O2 demand -> slow pulsate rate
Increase exercise tolerance -> decrease cardiac work
Preferred w arrhythmias -> negative ionotropic and chronotropic effects slow AV node conduction and increase AV refractory period
Slow ventricular response in Afib
Decrease ventricular beats
HTN - may be combined with diuretic, CCB, ACEI, ARB
Chronic use decreased BP due to decrease pulse rate, CO and renin release
Less effective for African Americans
Treatment for HFrEF
Carvediol (alpha 1, beta 1 + 2 antagonist)
Metropolol succinate - selective beta 1 antagonist
Bisprolol
Clinical concerns for Beta Blockers
Abrupt Cessation -> risk of angina/MI
Drug-drug interactions - consider other drugs with negative chrono/ionotropic effects = severe hypotension, bradycardia, CHF, conduction abnormalities, heart block
Adrenergic
SANA
Autonomic ganglia -> Nueronal nictonic receptors only -> ACH
Alpha and beta receptors -> NE/E - cardiac and SM cells, gland cells, nerve terminals
Adrenal medulla -> NE/E
Dopaminergic receptors (D) -> DA - renal vasc SM
Muscarinic receptors (M) -> ACH -> sweat glands
Adernergic transmission
- Tyrosine enters axon and is converted to dopamine (DA) via tyr hyroxylase
- DA transported into vessicle via VMAT where DA is converted -> NE via beta-hydroxylase
- NE released via exocytosis from influx of Ca2+ (VAMPS/SNAPS fuse)
- NE acts on post-synaptic and pre-synaptic receptors
- Noradrenergic transmission termination
- Metabolized via MAO, COMT inside axon, NET on aurtoreceptors