Adrenegic agents
Drugs that mimic or enhance actions of EP or NE
Direct acting agents
Activate adrenegic recptores
Indirect acting agents
No direct receptor actions
CAT inhibitors
monamine oxidase inhibitors
Adrenolitic agents
Block NE/EP actions
Chemical properties of catecholamines
Catechol ring
Oxidized in room air
Catecholamine drugs
Dopamine
Norepi.
Epin.
Isoproterenol
Properties of catecholamines
Not well absorbed
Rapid onset
Short duration
Enzymatic degradation
Two families of adrenegic receptors
Alpha
Beta
What receptors does Epi have a stronger action on
Beta
Norepi has stronger action on what receptors
Alpha
Where are alpha receptors located
Visceral organs
CNS
A1 effects
Increased PI formation
A2 effects
Decreased cAMP formation
Phenylephrine receptors
Alpha agonist
Beta receptor effects
Increase cAMP
Beta 1/2 agonist
Isoproterenol
What mediates EP and NE effects
B1 receptors in cardiac tissues
What effect do Symp drugs have on the heart
Increase: rate, contractility, conduction velocity
How do B1 receptors work
Via G protien mediated activation of adrenal cyclist with increased production of intracellular cAMP
Target of Symp stimulation on blood vessels
Vascular smooth muscle cell
Sympathetic effect on blood vessels
Pressor response
Increase mean arterial pressure
opposing actions by B and A receptors
A1 receptor on blood vessel
Increase blood receptor
Constriction
B2 receptor on blood vessels
Dilation
Cardiovascular actions of NE depend on
What receptor
A1 stimulation NE
Increased: systolic, diastolic, and mean arterial pressures
Decreased: Heart rate
Why does NE stimulation with a1 receptor cause a decrease in HR
Barroreceptors
Isoproterenol works on what receptors
Beta
Effect of Isoproterenol on B2
Decrease: blood pressure
vasodilation
Increase: heart rate, cardiac output
EP acts on
A2 and B1&2 receptors
EP low dose
B2: Vasodilation
B1: increase HR., cardiac output
EP high dose
B1: Increase HR (can cause arrhythmia)
B1 & A1: systolic vasoconstriction
A1: diastolic vasoconstriction
Eye a1 agonist
Pupil dilation
Lungs B2 agonists
Enhanced secretion
Relaxation
Used in inhalers
Lungs a1 agonist
Reduced secretion (predominates)
GI B1
Reduce motility
GI a1
Constrict sphincter
Bladder b1
Relax fundis
Bladder a1
Constict sphincter
Sweat glands
Goofy as shit
Uses of alpha adrenegic agonists
Maintain blood pressure
Reduce localized bleeding
Nasal decongestants
Emetic effect in cats
Phenylephrine
Increase BP
Acute pressor
-Management of shock
Stimulates a1&2
Phenylephrine adverse effects
Bradycardia
Excitation/nervous
PE + atropine = increased BP and tachycardia
Extravasation injury
A adrenegic antagonists uses
acute reduction in BP
Urinary tract disorders (relaxes)
Reversal of Xylazine induced depression
Side effects of alpha blocker
Postural hypotension GI irritability Stuffiness Impotence Sedation and depression
A- adrenergic antagonists
Phentolamine
Phenoxybenzamine
Yohimbine
Atipamezole
Use of B adrenergic agonists
B1: Acute treatment of cardiac failure B2: Respiratory difficulty and bronchial asthma -short term Delay parturition B1/2: allergic reactions
Uses for a adrenergic agonists
Hemostasis
Nasal decongestant
Raise BP
Adjuncts to local anesthetics
Isoproterenol
B1/2
Cardiac stimulation
Terbutaline
B2
Treat asthma
No stimulation of heart
B adrenergic agonists uses
Increase: HR, Cardiac contraction Conduction through AV node (B1)
Smooth muscle relaxation (B2)
What does the magnitude of effects produced by adrenegic drugs depend on
Sympathetic activity
Primary use for B antagonists
Cardiac effects
Long term control of systemic hypertension
Anti arrhythmic
Heart failure
Propranolol
B1/2
Antiarrhythmic
Must be withdrawn gradually
IV
Atenolol
B1 blocker
Anti arrhythmic
Esmolol
B1 blocker
