Drug name	broad class	specific class	receptor selectivity	clinical actions	toxicities	notes
Epinephrine	direct sympathomimetic	Catecholamine	all adr recep	brochodilation tretaing severe allergic reactions (brochospasm and hypotention) knocks out immune response by raising cAMP in mast cells used with local anestheics to produce local vasoconstriction and reduce escape of anthesthetic	decreased blood flow to the periphery, leading to necrosis of fingers and damge to periph tissues
norepinephrine	direct sympathomimetic	Catecholamine	a1, a2, b1
dobutamine	direct sympathomimetic	Catecholamine	B1 >>B2	+ ionontropic effects temporary support of myocardial function	increased mortatilty over long periods of time in cardiac failure patients	has bulky group on nitrogen leding to b1 selectivity and reduced metabolism by MAO
dopamine	direct sympathomimetic	Catecholamine	D1 dopaine receptor at high doses, B1 and A1 activation	important in CNS pharmacology - schizophrenia, Parkinson's disease vasoidilation of renal and mesenteric beds at low doses (renal sparing)	at high doses, lose renal sparing effect
phenylephrine	direct sympathomimetic	non-cachechol	a1 >> a2	good nasal decongestiant via vasoconstriction used as mydriatic -dilating pupil		can be taken orally longer acting
clonidine	direct sympathomimetic	non-cachechol	a2	acts in CNS acts peripherally, to inhibit NT release and extrajunctionally in vascular smooth muscle acts as anti-hypertensive used to treat withdraw symptoms by knocking down sympathetic activity	drowsiness and nasal congestion
albuterol	direct sympathomimetic	non-cachechol	B2>b1	asthmatic attack treatment	sudden death due to cardiac arrthmia due to b1 receptors	oral absoprtion
terbutaline	direct sympathomimetic	non-cachechol	B2>b1	asthmatic attack treatment	sudden death due to cardiac arrthmia due to b1 receptors	oral absorotpoin
amphetamine	indirect acting sympathomimetics			stimulates mass release of endogenous catechols from nerve terminal used to treat narcolepcy, ADHD, sometimes weight reduction	addictive, hypertensive crisis, MI, other profound sympathetic stimulatoin-mediated events
tyramine	indirect acting sympathomimetics				substrate for MAO. can cause hypertensive crsis when taken with MAO inhibitors.	is fermentation product present in wine, beer, cheese, yeast extracts
isoproterenol	direct sympathomimietic	catchecolamine	B1, B2	+ ionontropic effects by direct stimulatination of SA node	increased bood pressure, cardiac failure, not much used clnically
alpha methyl dopa	a2 selective agonist		a2	reduced blood pressure by conversion to alpha methylnorepinepherine and unusual mech 18.5	drowsiness and nasal congestion
ephederine	mixed and directly acting sympathmimetics			increased BP, HR	present in ma Huang, can lead to problems
phenylpropanolamine	mixed and directly acting sympathmimetics					found in over the counter cold remedies
phenoxybenzmine	non-selective a-adr. blocker	irreversible	a1, a2 inhibitor	treats pheochromacytoma, longer half-life		key structure is chloroethyl group 19.2
phentolamine	non-selective a-adr. blocker	reversible	a1, a2 inhibitor	vasodilation, declreased blood pressure	can lead to uncontrolled tachycardia (19.3) and postural hypotention
prazosin	selective a-adr. blocker		a1 selective inhibitor	will block a1 and stop hypertension, but leaves a2 intact allowing control of heart rate. leads to symptomatic relief for prostatic hypertrophy
yohimbine	selective a-adr. blocker		a2 selective inhibitor	treats impotence by blocking a2 feedback, allowing increased cachechol release	seizures, increase bp and hr
propranolol	non-selective b-blockers		b1, b2 inhib	decreases heart rate, excessive sympathteic stimulatoin.		readily but higly variably metabolized in liver ½ life of 3 - 4 hrs.
nadolol	non-selective b-blockers		b1, b2 inhib	decreases heart rate, excessive sympathteic stimulatoin.		cleared by kidney ½ life of 20 hrs
timolol	non-selective b-blockers		b1, b2 inhib	decreases heart rate, excessive sympathteic stimulatoin. used to treat glaucoma		cleared by liver ½ life of 4 hours
metoprolol	selective b-blockers		b1 > b2 inhib	decreases heart rate, excessive sympathteic stimulatoin.		cleared by liver ½ life of 4 hours
atenolol	selective b-blockers		b1 > b2 inhib	decreases heart rate, excessive sympathteic stimulatoin.		renal clearance ½ life of 12 hours
pindolol	non-selective b-blocker	partial agonist ability	b1, b2 inhib	blocks b activity while still having some agonist, thus preventing prfound depression of hr and cardiac output.
labetalol	non-selective b-blocker	with some a1 antagonist activity	b1, b2 inhib a1 antagonist
carbamylcholine	cholinergic agonist	choline ester		used to open outflow tract in glaucoma given to treat post-operative gastric atony used to treat bladder paraylsis	major contraindication against asthma, because they cause bronchoconstriction induces excess acid production risk of hyoptension	other than AcH, many are resistanct to actions of cholinesterase (like carbamylcholine)
bethanechol	cholinergic agonist	choline ester	muscarnic receptor selective		major contraindication against asthma, because they cause bronchoconstriction induces excess acid production risk of hyoptension	not degraded well by CE
pilocarpine	cholinergic agonist	alkaloid			major contraindication against asthma, because they cause bronchoconstriction induces excess acid production risk of hyoptension	absorbed topically
atropine	muscarinic antagonist	non-selective	all muscarnics			is a teritary amine, so can be administered via GI and act on CNS
scopolamine	muscarinic antagonist	non-selective	all muscarnics			is a teritary amine, so can be administered via GI and act on CNS
ipratropium	muscarinic antagonist	non-selective	all muscarnics	used mostly for asthma		quaternary amines
propantheline	muscarinic antagonist	non-selective	all muscarnics	given orally for mostly GI uses		quaternary amines
pirenzipine	muscarinic antagonist	m1 selective	m1	controlls acid release in peptic ulcer disease
physostigmine	acetylcholinesterase inhibitors	carbamate inhibitor	ach esterase	galucoma treatment to increase muscarinic action myasthenia gravis reversal of neuromuscular blockade treating atropine poisioning		is a tertiary amine so it enters brain easily acts by carbamylating enzyme, which returns to normla much slower than acetylated as normal
neostigmine	acetylcholinesterase inhibitors	carbamate inhibitor	ach esterase	galucoma treatment to increase muscarinic action myasthenia gravis reversal of neuromuscular blockade treating atropine poisioning	cannot use with depoliarizing nicotinic antagoinists (worsens block)	quatrenary amine, so action confined to periphery
edrophonium	acetylcholinesterase inhibitors	competitive inhibitor	ach esterase	galucoma treatment to increase muscarinic action myasthenia gravis reversal of neuromuscular blockade treating atropine poisioning		acts simply by competing with ACh for slots
sarin and somin	acetylcholinesterase inhibitors	irreversible inhibitor, organophosphorus inhibitor
diphenhydramine	Primarily anti-histamine (secondarily) anti-muscarinic
amitrytiline	tricyclinc anti-depressant and also anti-muscarinic
curare	nicotinic antagoinist	non-depolarizing (competitive antagoinst)	Nm, Ng		histamine release	quaternary structure, not absorbed across GI renal clearance (long action)
hexamethonium	nicotinic antagonist	more specific for Ng	Ng	used for Gillian-Barre syndrome	causes massive blockade everywhere of multiple effects
Baclofen	gaba agonist		GABA	muscle relaxation via CNS
Benzodiazepines	gaba agonist		GABA along with neurotransmitter
Dantrolene			blocks Ca++ release in cell	muscle relaxation and inhibition
pancuronium	nicotinic antagoinist	non-depolarizing (competitive antagoinst)	Nm, Ng	general anesthesia for total muscle block	prolonged respiratory depression	quatrenary compound renal excretion long clearnace
atracurium	nicotinic antagoinist	non-depolarizing (competitive antagoinst)	Nm, Ng	general anesthesia for total muscle block	prolonged respiratory depression	quatrenary compound intermediate duration
mivacurium	nicotinic antagoinist	non-depolarizing (competitive antagoinst)	Nm, Ng	general anesthesia for total muscle block	prolonged respiratory depression	quatrenary compound short action
succinylcholine	nicotinic antagoinsist	depolarizing, initial activation with later deactivation	Nm	general anesthesia for total muscle block; very fast onset, decay	prolonged respiratory depression fasiculations (characteristic of non-depolarizing)	two acetylcholine molecules back to back short action extremely fast action

Receptors acted upon	Drug Class	Pharmacokinetics	actions	toxicities	administration
alpha agonist	Catecholamines	metabolized by MAO and COMT		can be toxic for those taking MAO inhibitors patients on b blockers will have dramatic vasoconstriction	Only parentally
alpha agonist	non-cachecholamines				orally
beta antagonists			decrease heart rate by blocking cachecholaine induced accel of spontaneous depol decrease automaticity decrease contractility increase lifetime of congestive heart failure patients	bradycardia, CnS effecs, blockated of B2 elead to brochospasm lead to decrease in glucose metabolisum/mobilization and are also contraindicated for diabetics
muscarinic agonists			drop rate of contraction and conduction velocity causes vasodilation of erictile tissues causes broncho constriction and increased secretion from glands causes increase in digetstive enzymes, secretion of stomach acid, and peristalsis increase in bladder function pupillary constrictuion and accomidation increases in salivary and lacrimal glands	asmha (causes bronchoconstrictuion)
muscarninic antagonists			decreased salivation bronchodilation tachycardia, with paradoxical bradycardia at low doses due to cns effects extensive cns effects pupillary dilation Used to treat parkinsons, motion skickness, peptic ulcers, sinus bradycardia, ashma, opthamiolic diagnostic dilation, uveitis, and antidote to mushrooms or poisn gas	hallucinations at higher cns doses gluacoma and prostate hypertrophy are major contraidications
acetylcholinesterase inhibitors		increase concentration of ach in synapses
nicotininc antagonists	non-depolarizing	Nm and Ng
nicotininc antagonists	depolarizing	Nm		causes faciculations

CREATED BY JEFFREY HUO, MAY 10TH 1998