ccb 2 Flashcards
calcium is important in
contraction of vascular smooth muscles, skeletal muscle and heart muscle
blocking ca channels causes
decrease influx into cell, decreased action
ca and myocytes
ca binds to troponin, links to crossbridging and pulls filaments which equals contraction
smooth muscle and calcium
binds to camodulin causing actin and myosin interaction- both require by g protein and ac activation and camp/ip3 activity
increased ca in cell from
increased influx and increased release from SR
camp acts as an
2nd messenger- increased CAMP causes an increase in intracellular calcium
what breaks down camp
phosphodiestarase
phosphodiesterase inhibitor does what
increases intracellular calcium and increases contraction
more phosphodiesterase
more breakdown camp
how is calcium activated and exert effect
excitation coupling
which ccb suppresses AV node the most
verapamil
what does verapamil do to heart rate
marked decrease
what ccb decreases heart rate second most
diltiazem
which ccb have no decrease in hr
dihydrapyradines- DHP- nifedipine, nicardipine, clevidipine
what does niffedipine do to HR
marked increase secondary to baroreceptor
NON DHP effects
negative inotropic (decrease contractility) negative chronotropic (decrease HR) negative dromotropy (decrease conduction negative lusitropy(relax heart)
what is the difference between nodal and myocyte action potential
nodal have automaticity, dont need stimulation like myocytes do on own
where does automaticity occur on nodal tissue
phase 4- mostly ca entering cell, some na
what would happen in phase 4 if block calcium channel into cell
decrease action potential, decrease HR
what phase of nodal tissue does ccb cause negative chronotropic effect
4
what phase does ccb cause negative inotropic effects
phase 2 on myocyte cell- not on nodal cell
ccb do what to coronary arteries?
dilate
what can ccb cause
coronary steal
why is cardizem better then nifedipine for ischemic patient
decrease HR, increase filling time gives more time for coronary perfusion
