-V-W Class III antiarrhythmics

-oral hypoglycemic agents

act at phase 3 (falling) of AP (during repolarization)

prolong refractory period

-tilide

I: Na Channel Blocker

II: beta-blocker

III: K Channel Blocker

IV: Ca Channel Blocker

dirty drug

class X: 1+2+3+4

mostly at K channel, but also others

commonly used

efficacious anti-arrhythmic

almost exclusive biliary excretion

half life approx 58 days

can cause everything: increase or decrease thyroid

less toxic amiodarone

no thyroid fx

non selective beta blocker...

main mode of antiarrhythmic is K channel blockade

mixture of isomers: d (class III) and l (class II and III)

induced by too much K blockade

overdose yields long (650ms) QT, diarrhythmia, treat with magnesium

all class III drugs torsadogenic, as well as Ia

oral hypoglycemic agents

block K channels in pancreas

causes depolarization, insulin release

gli-

side effects: weight gain, hypoglycemia

oral hypoglycemic, but not sulfonylurea

Metformin improves hyperglycemia primarily through its suppression of hepatic glucose production

Exact mechanism ?
Not via KCB

1st line, safe drug

oral hypoglycemic agents, not SUs

increase insulin release

bind to different site of K channel

ROSA

less side effects

cause hyperpolarization

-vascular (arterial) relaxation

-hair growth

arterial relaxation (afterload decrease, decrease O2 consumption)
treatment and prophylaxis of angina
congestive heart failure
hypertension

also stimulates cGMP via NO

causes oral ulcers :(