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20 Cards in this Set

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The alpha 1 receptor is a ___ GPCR and mediates [organ action] when stimulated.
Gq
smooth muscle contraction
The alpha 2 receptor is a ___ GPCR and mediates [organ action] when stimulated.
Gi
NT inhibitor, cardiac muscle relaxer
The beta 1 receptor is a ___ GPCR and mediates [organ action] when stimulated.
Gs
Cardiac muscle contractor
The beta 2 receptor is a ___ GPCR and mediates [organ action] when stimulated.
Gs
Smooth muscle relaxer
The beta 3 receptor is a ___ GPCR and mediates [organ action] when stimulated.
Gs
Fat cell lipolysis
Nicotinic Acetylcholine Receptors -- where and what kind?
Ionotropic / ligand-gated ion channel on skeletal muscle
Acetylcholine -- synthesis and degradation
Choline + AcetylCoA -----(aceteyltransferase) --- > Acetylcholine + CoA in nerve terminal

Acetylcholine + ACh esterase ----> choline + AcetylCoA at NMJ
Muscarinic AC Receptors
Metabotropic, GPCRs on the heart and smooth muscle and sweat glands
Name 2 non-selective beta-blockers
Alprenelol (Gubernal®)
Pindolol (Visken®)
Propranolol (Inderal®)
Sotalol (Betapace®)
Timolol (Blocadren®)
Name at least 2 beta-1 specific blockers.
Acebutolol (Sectral®)
Atenolol (Tenormin®)
Betaxolol (Betoptic®)
Esmolol (Brevibloc®)
Metoprolol (Lopressor®)
Name the three subtypes of calcium channel antagonists
Phenylakylamines (PHA)
Benzothiazepines (BNZ)
Dihydropyridines (DHP)
What do calcium channel antagonists do?
Inhibit L-type Ca2+ channels in myocardium and VSM.
What do beta blockers do?
Lower heart rate, lower cardiac output, reduce preload/afterload, lower oxygen demand
What's an example of PHA?
Verapamil
What's an example of BNZ?
Diltiazem
What's an example of a dihydropyridine (DHP)?
Amlodipine
Nicardapine
What Calcium channel subtype affects the heart the strongest?
PHA > BNZ >>> DHP
What Calcium channel subtype affects the VSM the strongest?
DHP >>> PHA=BNZ
Mechanism of action of Ca+ channel blockers on heart.
↓Ca2+ influx during cardiac AP → ↓ conduction velocity → ↓ HR → ↓ CO → ↓ myocardial O2 demand
Mechanism of action of Ca+ channel blockers on VSM.
↓Ca2+ influx following GPCR activation → ↓ MLCK activity → ↓ vascular tone → ↓ afterload