Foundations 1 Flashcards
Primary NT involved in somatic nervous system
Acetylcholine (Ach)
What receptor does Ach bind to in skeletal muscles to affect muscle movement?
Nicotinic receptors
What NT does the parasympathetic nervous system release, what receptor does it bind to, and what response does the binding cause?
ACh
Muscarinic receptors (GI tract, bladder, and eyes)
SLUDD
SLUDD
Salivation, lacrimation, urination, defecation, and digestion
What are the main NTs released by the sympathetic nervous system, what receptors do these bind to, and what response occurs due to this binding?
Epinephrine and norepinephrine
Adrenergic receptors
Increased BP, HR, and bronchodilation
Where are alpha 1 receptors located?
Smooth muscles (e.g., blood vessels)
Where are beta 1 receptors located?
Heart
Where are beta 2 receptors located?
Lungs and GI tract
Antagonists binds to SAME ACTIVE SITE of receptor as the endogenous substrate —> prevents substrate from binding —> reaction
Competitive inhibition
Antagonist binds to receptor at a site other than the active site (ALLOSTERIC SITE) —> shape of active site changes —> prevents endogenous substrate from binding
Non-competitive inhibition
MUSCARINIC RECEPTOR
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: ACh
Agonist action: Increases SLUDD
Drug agonists: Pilocarpine, bethanechol
Antagonist action: Decreases SLUDD
Drug antagonists: Atropine, oxybutynin
NICOTINIC RECEPTOR
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: ACh
Agonist action: Increased BP, HR
Drug agonists: Nicotine
Antagonist action: Neuromuscular blockade
Drug antagonists: Neuromuscular blockers (rocuronium)
ALPHA-1 (mainly peripheral)
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: Epi, NE
Agonist action: Smooth muscle vasoconstriction, increased BP
Drug agonists: Phenylephrine, dopamine (dose-dependent)
Antagonist action: Smooth muscle relaxation, decreased BP
Drug antagonists: Alpha 1 blockers (doxazosin, carvedilol, phentolamine)
ALPHA 2 (mainly brain; central)
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: Epi, NE
Agonist action: Decreased release of Epi and NE, decreased BP and HR
Drug agonists: Clonidine, brimonidine (ophthalmic for glaucoma)
Antagonist action: Increased BP, HR
Drug antagonists: Ergot alkaloids, yohimbine
BETA 1 (mainly heart)
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: Epi, NE
Agonist action: Increased myocardial contractility, CO, HR
Drug agonists: Dobutamine, isoproterenol, dopamine (dose-dependent)
Antagonist action: Decreased CO, HR
Drug antagonists: Beta blockers
BETA 2 (mainly lungs)
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: Epi
Agonist action: Bronchodilation
Drug agonists: Albuterol, terbutaline, isoproterenol
Antagonist action: Bronchoconstriction
Drug antagonists: Non-selective beta blockers (propranolol, carvedilol)
DOPAMINE
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: Dopamine
Agonist action: Renal, cardiac, and CNS effects
Drug agonists: Levodopa, pramipexole
Antagonist action: Renal, cardiac, and CNS effects
Drug antagonists: 1st generation antipsychotics (haloperidol) and metoclopramide
SEROTONIN
Endogenous substrate:
Agonist action:
Drug agonists:
Antagonist action:
Drug antagonists:
Endogenous substrate: Serotonin
Agonist action: Platelet, GI, and psychiatric effects
Drug agonists: Triptans (sumatriptan)
Antagonist action: Platelet, GI, and psychiatric effects
Drug antagonists: Ondansetron, 2nd generation antipsychotics (quetiapine)
ACETYLCHOLINESTERASE
Endogenous effects:
Drug examples:
Drug action:
Endogenous effects: Breaks down ACh
Drug examples: Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine)
Drug action: Blocks acetylcholinesterase —> increases ACh levels; used to treat Alzheimer’s disease
Angiotensin-converting enzyme (ACE)
Endogenous effects:
Drug examples:
Drug action:
Common uses:
Endogenous effects: Converts angiotensin I to angiotensin II (potent vasoconstrictor)
Drug examples: ACE inhibitors
Drug action: Inhibit production of angiotensin II —> decreases vasoconstriction and aldosterone secretion
Common uses: Used to treat HTN, HF, and kidney
Catechol-O-methyltransferase
Endogenous effects:
Drug examples:
Drug action:
Common uses:
Endogenous effects: Breaks down levodopa
Drug examples: COMT inhibitor (ent a sponge)
Drug action: Blocks COMT enzyme to prevent peripheral breakdown of levodopa —> increases duration of action of levodopa
Common uses: Parkinson’s disease
Cyclooxygenase (COX)
Endogenous effects:
Drug examples:
Drug action:
Common uses:
Endogenous effects: Converts arachidonic acid to prostaglandins (cause inflammation) and thromboxane A2 (causes platelet aggregation)
Drug examples: NSAIDS
Drug action: Block COX to decrease prostaglandins and thromboxane A2
Common uses: Treat pain/inflammation and decrease platelet activation/aggregation (aspirin)
Monoamine oxidase (MAO)
Endogenous effects:
Drug examples:
Drug action:
Common uses:
Endogenous effects: Breaks down catecholamines (DA, NE, Epi, 5-HT)
Drug examples: MAO inhibitors (phenelzine, tranylcypromine, isocarboxazid, selegiline, rasagiline, methylene blue, linezolid)
Drug action: Block MAO —> increases catecholamine levels
Common uses: Depression
**Increasing catecholamines too much can cause toxicity (hypertensive crisis, serotonin syndrome)
Phosphodiesterase (PDE)
Endogenous effects:
Drug examples:
Drug action:
Common uses:
Endogenous effects: Breaks down cGMP (smooth muscle relaxant)
Drug examples: PDE-5 inhibitors (sildenafil, tadalafil)
Drug action: Competitively bind to same active site as cGMP on the PDE-5 enzyme —> prevents breakdown of cGMP and prolong smooth muscle relaxation
Common uses: Erectile dysfunction