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CALCIUM CHANNEL
BLOCKERS
MEDICAL STUDENT: MOHAMMAD TAILAKH .
4TH YEAR AT JU.
CCB
• It has been known since the late 1800s that transmembrane calcium influx is
necessary for the contraction of smooth and cardiac muscle. The discovery of a
calcium channel in cardiac muscle was followed by the finding of several different
types of calcium channels in different tissues.
• Although the blockers currently available for clinical use in cardiovascular
conditions are exclusively L-type calcium channel blockers.
Type Channel Name Where Found Properties of the
Calcium Current
Blocked By
L CaV1.1–CaV1.3 Cardiac, skeletal,
smooth muscle,
neurons (CaV1.4 is
found in retina),
endocrine cells, bone
Long, large, high
threshold
Verapamil, DHPs,
Cd2+, -aga-IIIA
T CaV3.1–CaV3.3 Heart, neurons Short, small, low
threshold
sFTX, flunarizine,
mibefradil1
N CaV2.2 Neurons, sperm2
Short, high threshold Ziconotide,3 gabapen
tin,4 -CTX-
GVIA, -aga-IIIA,
Cd2+
P/Q CaV2.1 Neurons Long, high threshold -CTX-MVIIC, -
aga-IVA
CCB
• They divided into three chemical classes:
• a. Diphenylalkylamines, Varapamil.
• b. Benzothiazepines, Diltiazem
• c. Dihydropyridines, Nifedipine
• MECHANISM OF ACTION
• Calcium enters muscle cell through special voltage sensitive calcium channel.
• Normally, L-Type of channels admit Ca+ and causes depolarization – excitation-
contraction coupling through phosphorylation of myosin light chain – contraction
of vascular smooth muscle – elevation of BP CCBs block L-Type
• These agents exert their effect by antagonists block
for the inward movement of calcium by
binding to the L-type channels
in the heart and peripheral vasculature
ORGAN SYSTEM EFFECTS
• 1. Smooth muscle: dependent on transmembrane calcium influx for
normal resting tone and contractile responses.
• Vascular smooth muscles (most sensitive) relaxed by the calcium channel
blockers.
• reduction in peripheral vascular resistance .
• Reduction of coronary artery spasm .
2. CARDIAC MUSCLE
• Normally: highly dependent on calcium influx during each action potential for
normal function(plateau).
• Impulse generation in the sinoatrial node and conduction in the atrioventricular
node.
• reduce cardiac contractility , decrease CO, reduce oxygen requirement in with
angina.
3. SKELETAL MUSCLE
• Skeletal muscle is not depressed by the calcium channel blockers because it
uses intracellular pools of calcium to support excitation-contraction coupling
and does not require as much transmembrane calcium influx.
CLINICAL EFFECTS
• decrease myocardial contractile force.
• reduces myocardial oxygen requirements.
• Decrease peripheral resistance .
• Decreased heart rate with the use of verapamil or diltiazem causes a further
decrease in myocardial oxygen demand.
NIFEDIPINE DILTIAZEM VERAPAMIL
coronary arteries
dilation
++ ++ ++
peripheral
arteries dilation
++++ ++ +++
negative
inotropic
+ ++ +++
slowing AV cond  +++ ++++
heart rate      
↓ blood pressure ++++ ++ +++
depression of SA
increase in
cardiac
output

++
++

++

INDICATIONS
• Angina.
• Hypertension.
• Raynaud's phenomenon. (Nifedipine is the mainstay of medical treatment).
• Supraventricular tachycardias, including atrial fibrillation.
• Ischaemic neurological deficit after subarachnoid haemorrhage.
• Delay of preterm labour(prevent premature labour has been with nifedipine)
• Prophylaxis for cluster headache.
USAGE
• Verapamil and Diltiazem are used in arrhythmias because they have an effect on the
heart. They both are not great antihypertensive drugs
• because they have negative inotropic and chronotropic effects,
• however are used in patients who have palpitations/arrhythmias and suffer from HTN
since they can reduce heart rate and blood pressure simultaneously.
• Dihydropyridines: depend on JNC-8, found in first line theraby espically in black
population have a high efficacy of 40 mmHg, regarding that the highest reduction in
blood pressure an orally taken anti-hypertensive drug can cause is 40 mmHg.
ADVERSE EFFECTS
• Common adverse effects
• These can be predicted from the type of CCB and mode of action, as already illustrated.
Examples include:
• Myocardial effects
• Hypotension
• Heart failure
• Conduction effects
• Heart block
• Arrhythmias
ADVERSE EFFECTS
• Vascular smooth muscle
• Flushing
• Oedema
• Headaches
• Rashes
• Other effects
• Constipation
• Rashes
• Gynaecomastia
• Photosensitivit
ADVERSE EFFECTS
drug Effect on heart rate Adverse effect
Nifedipine  Headache, flushing, ankle
swelling
Amlodipine  Ankle swelling, Gingival
hyperplasia
Nimodipine ± Flushing, headache
Diltiazem ± Generally mild
Verapamil  Constipation, marked
negative
inotropic action
CAUTIONS AND CONTRA-INDICATIONS
• Again, these can be predicted from the type of CCB and mode of action.
Individual drug monographs need to be reviewed. Some examples include:
• Cardiovascular: shock, unstable angina, significant aortic stenosis, bradycardia,
heart failure, etc.
• Avoidance of grapefruit juice with felodipine, lacidipine, lercanidipine, nicardipine,
nifedipine, nimodipine and verapamil. This may affect metabolism.
• Sudden withdrawal of CCBs may exacerbate angina.
• These are best considered under each individual drug.
Calcium channel blockers

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Calcium channel blockers

  • 1. CALCIUM CHANNEL BLOCKERS MEDICAL STUDENT: MOHAMMAD TAILAKH . 4TH YEAR AT JU.
  • 2. CCB • It has been known since the late 1800s that transmembrane calcium influx is necessary for the contraction of smooth and cardiac muscle. The discovery of a calcium channel in cardiac muscle was followed by the finding of several different types of calcium channels in different tissues. • Although the blockers currently available for clinical use in cardiovascular conditions are exclusively L-type calcium channel blockers.
  • 3. Type Channel Name Where Found Properties of the Calcium Current Blocked By L CaV1.1–CaV1.3 Cardiac, skeletal, smooth muscle, neurons (CaV1.4 is found in retina), endocrine cells, bone Long, large, high threshold Verapamil, DHPs, Cd2+, -aga-IIIA T CaV3.1–CaV3.3 Heart, neurons Short, small, low threshold sFTX, flunarizine, mibefradil1 N CaV2.2 Neurons, sperm2 Short, high threshold Ziconotide,3 gabapen tin,4 -CTX- GVIA, -aga-IIIA, Cd2+ P/Q CaV2.1 Neurons Long, high threshold -CTX-MVIIC, - aga-IVA
  • 4. CCB • They divided into three chemical classes: • a. Diphenylalkylamines, Varapamil. • b. Benzothiazepines, Diltiazem • c. Dihydropyridines, Nifedipine
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  • 6. • MECHANISM OF ACTION • Calcium enters muscle cell through special voltage sensitive calcium channel. • Normally, L-Type of channels admit Ca+ and causes depolarization – excitation- contraction coupling through phosphorylation of myosin light chain – contraction of vascular smooth muscle – elevation of BP CCBs block L-Type • These agents exert their effect by antagonists block for the inward movement of calcium by binding to the L-type channels in the heart and peripheral vasculature
  • 7. ORGAN SYSTEM EFFECTS • 1. Smooth muscle: dependent on transmembrane calcium influx for normal resting tone and contractile responses. • Vascular smooth muscles (most sensitive) relaxed by the calcium channel blockers. • reduction in peripheral vascular resistance . • Reduction of coronary artery spasm .
  • 8. 2. CARDIAC MUSCLE • Normally: highly dependent on calcium influx during each action potential for normal function(plateau). • Impulse generation in the sinoatrial node and conduction in the atrioventricular node. • reduce cardiac contractility , decrease CO, reduce oxygen requirement in with angina.
  • 9. 3. SKELETAL MUSCLE • Skeletal muscle is not depressed by the calcium channel blockers because it uses intracellular pools of calcium to support excitation-contraction coupling and does not require as much transmembrane calcium influx.
  • 10. CLINICAL EFFECTS • decrease myocardial contractile force. • reduces myocardial oxygen requirements. • Decrease peripheral resistance . • Decreased heart rate with the use of verapamil or diltiazem causes a further decrease in myocardial oxygen demand.
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  • 13. NIFEDIPINE DILTIAZEM VERAPAMIL coronary arteries dilation ++ ++ ++ peripheral arteries dilation ++++ ++ +++ negative inotropic + ++ +++ slowing AV cond  +++ ++++ heart rate       ↓ blood pressure ++++ ++ +++ depression of SA increase in cardiac output  ++ ++  ++ 
  • 14. INDICATIONS • Angina. • Hypertension. • Raynaud's phenomenon. (Nifedipine is the mainstay of medical treatment). • Supraventricular tachycardias, including atrial fibrillation. • Ischaemic neurological deficit after subarachnoid haemorrhage. • Delay of preterm labour(prevent premature labour has been with nifedipine) • Prophylaxis for cluster headache.
  • 15. USAGE • Verapamil and Diltiazem are used in arrhythmias because they have an effect on the heart. They both are not great antihypertensive drugs • because they have negative inotropic and chronotropic effects, • however are used in patients who have palpitations/arrhythmias and suffer from HTN since they can reduce heart rate and blood pressure simultaneously. • Dihydropyridines: depend on JNC-8, found in first line theraby espically in black population have a high efficacy of 40 mmHg, regarding that the highest reduction in blood pressure an orally taken anti-hypertensive drug can cause is 40 mmHg.
  • 16. ADVERSE EFFECTS • Common adverse effects • These can be predicted from the type of CCB and mode of action, as already illustrated. Examples include: • Myocardial effects • Hypotension • Heart failure • Conduction effects • Heart block • Arrhythmias
  • 17. ADVERSE EFFECTS • Vascular smooth muscle • Flushing • Oedema • Headaches • Rashes • Other effects • Constipation • Rashes • Gynaecomastia • Photosensitivit
  • 18. ADVERSE EFFECTS drug Effect on heart rate Adverse effect Nifedipine  Headache, flushing, ankle swelling Amlodipine  Ankle swelling, Gingival hyperplasia Nimodipine ± Flushing, headache Diltiazem ± Generally mild Verapamil  Constipation, marked negative inotropic action
  • 19. CAUTIONS AND CONTRA-INDICATIONS • Again, these can be predicted from the type of CCB and mode of action. Individual drug monographs need to be reviewed. Some examples include: • Cardiovascular: shock, unstable angina, significant aortic stenosis, bradycardia, heart failure, etc. • Avoidance of grapefruit juice with felodipine, lacidipine, lercanidipine, nicardipine, nifedipine, nimodipine and verapamil. This may affect metabolism. • Sudden withdrawal of CCBs may exacerbate angina. • These are best considered under each individual drug.