Unit 3- Adrenergic Antagonists Flashcards
Prazosin Selectivity
α1
Phenoxybenzamine Selectivity
α1
Phentolamine Selectivity
α
Antipemezole Selectivity
α2
Yohimbine Selectivity
α2
Carvedilol Selectivity
β>α1
Propanolol Selectivity
β
Timolol Selectivity
β
Metoprolol Selectivity
β1
α Antagonist Structure
Diverse, competitive antagonists
Phenothiazine Tranquilizers
α antagonists blocking receptors, causing decrease in peripheral vascular resistance
α Antagonist Cardiovascular
Dilate vessels
EPI Reversal Effect
Pretreating with α1 antagonists to reduce peripheral vascular resistance due to EPI
α1 Antagonist Effects
Decrease resistance to urine flow
α2 Antagonist Effects
Antiplatelet aggregation, stimulate insulin, reverse sedation
α Antagonist Effects
3rd eyelid protrusion, miosis, nasal stuffiness
Nonselective α Antagonists
Phenoxybenzamine, phenothiazine tranquilizers, and trazodone
Phenoxybenzamine
Irreversibly blocks α receptor to inhibit NE reuptake, antagonizes histamine, Ach, and serotonin receptors, manages catecholamine excess
Selective α1 Antagonists
Prazosin, tamsulosin, silodosin
Prazosin
Vessel dilation, decrease urine flow, reduces urethral pressure, decreases MAP
Tamulosin
Higher affinity for urethra and prostate than vascular smooth muscle, decreases intraurethral pressure
Silodosin
Decreases intraurethral pressure
Selective α2 Antagonists
Reverse sedative effects of α2 agonists; yohimbine, tolazoline, atipamezole
Yohimbine
Increases NE release to cause stimulation, HR increase, and BP increase, increases GI motility, antagonizes serotonin receptors
Tolazoline
α antagonist to reverse xylazine and other α2 agonists in horses
Atipamezole
Reverses α2 agonist sedation, effective in all species, mostly used in small animal
α Agonist Sedatives
Block presynaptic α receptors, suppressing NE release via negative feedback
β Antagonist Cardiovascular Effects
Decreases cardiac output, can lower BP
β Antagonist Pulmonary Effects
Bronchoconstriction and increased airway resistance
β Antagonist Ophthalmic Effects
Reduce intraocular pressure by decreasing aqueous humor production
β Antagonist Metabolic Effects
Inhibit lipolysis and glycogenolysis, delay recovery from hyperglycemia
First Gen β Antagonists
Nonselective, propanolol
Second Gen β Antagonists
β1 selective, metoprolol, atenolol, esmolol
Third Gen β Antagonists
Nonselective with additional cardiovascular effects, carvedilol
Propanolol
Competitive antagonist blocking receptors, decreases HR and cardiac output, decreases oxygen demand, increases airway resistance
Propanolol Uses
Treats tachyarrhythmia, hypertension, cardiomyopathy, and thyrotoxicosis
Propanolol Side Effects
Upregulation of β receptors, excess β stimulation with abrupt stop of treatment, bronchospasm
Metoprolol
Blocks β2 receptors, decreases HR and cardiac output, decreases oxygen demand, reduces BP, inhibits agonist induced tachycardia
Metoprolol Uses
Tachyarrhythmia, premature contraction, hypertension, hypertrophic cardiomyopathy, thyrotoxicosis, safe in asthmatics
Atenolol
Decreases HR and cardiac output, decreases MAP
Atenolol Uses
Arrhythmia, hypertension, hypertrophic cardiomyopathy
Atenolol Side Effects
Can block β2 receptors, not for asthmatics, reduces cardiac output, lethargy, hypotension, diarrhea
Esmolol
Ultra short acting
Esmolol Uses
Tachyarrhythmia, ventricular outflow obstruction
Esmolol Side Effects
Significant cardiac output reduction
Carvedilol
β blocker, some α1 antagonism, vasodilator, free radical scavenger
Carvedilol Uses
Anti arrhythmic, dilated cardiomyopathy and chronic valve disease
Chronic Mitral Valvular Disease
Most common cause of heart disease and CHF in dogs, treated with carvedilol
Hypertrophic Cardiomyopathy
Most common heart disease in cats, treated with atenolol
Subaortic Stenosis
Congenital cardiac abnormality in dogs, treated with atenolol