''VERY NICE DRUGS''
V - Verapamil
N - Nifedipine
D - Diltiazem
CCBs can be subdivided according to structural and functional distinctions.
A - amlodipine,
N - nicardipine, nifedipine, nisoldipine
2. Phenylalkylamine : verapamil
3. Benzothiazepine: diltiazem
Calcium & muscle contraction
voltage gated calcium channel (VGCC) located in the cells that undergo depolarisation eg muscles, glial cell, neurone--> lead to muscle contraction.
calcium is stored in the sarcoplasmic reticulum,
Tropomyosin is coiled around the actin filament by the help of another protein known as troponin.
in the other words, troponin we said it is attached to tropomyosin.
Tropomyosin functions to prevent myosin from binding to the actin filament.
To unblock it( allow myosin attached to actin filament) --> troponin need change its shape and conformation.
How troponin can change its shape? Good questions??
When calcium ion present in high conc., calcium ion will bind to troponin and move the tropomyosin ''out of way'' and push actin filament to the right side.
once the calcium ion bound to troponin & troponin change its shape, the myosin able to bind to actin filament and finally lead to muscle contraction.
after sometimes, calcium ions become lesser. Low conc of calcium get released from troponin. Troponin then goes back to its original shape, make tropomyosin block myosin again.
- Prevent calcium ion ( for muscle contraction) from entering into smooth and cardiac muscle cells.
- thus, it lower systolic & diastolic BP --> reduce angina.
- Some CCBs eg. Procaine( nifedipine) slow electrical impulse that run through heart muscle, it helps to regulate arrhythmia.
clinical apps of CCB
C - Congestive Heart Failure
H - HTN
S- Supreventricular tachyarrthymias
M- Migraine (same as beta blockers)
A- Atrial flutter / atrial fibrillation
IMPORTANT = CCBs is DOC for atrial flutter/ atrial fibrillation.
Caution should be taken when using verapamil with a beta blocker due to the risk of severe bradycardia.