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![CCBs Act Selectively on Cardiovascular Tissues
• Neurons rely on N-and P-type Ca2+ channels
• Skeletal muscle relies primarily on [Ca]
• Cardiac muscle requires Ca2+ influx through L-type
Ca2+ channels
• contraction (fast response cells)
• upstroke of AP (slow response cells)
• Vascular smooth muscle requires Ca2+ influx through
L-type Ca2+ channels for contraction](https://image.slidesharecdn.com/ccb-190608060507/75/calcium-channel-blocker-16-2048.jpg)
Uploaded byDr. Rupendra Bharti
calcium channel blocker
Calcium channel blockers (CCBs) are a class of drugs that inhibit the movement of calcium ions across cell membranes. There are three main classes of CCBs: dihydropyridines like nifedipine, phenylalkylamines like verapamil, and benzothiazepines like diltiazem. CCBs work by blocking L-type calcium channels in cardiac and vascular smooth muscle cells, which decreases calcium entry and inhibits contraction. This leads to vasodilation, reduced peripheral resistance, and decreased blood pressure and workload on the heart. Common uses of CCBs include hypertension, angina, arrhythmias, and migraines. Adverse effects vary between classes but can
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Introduction to CCBs and their basic classification.
Verapamil, Nifedipine, and Diltiazem; their properties and significance in treating conditions.
Types of calcium channels: voltage sensitive, receptor-operated, and leak channels.
How CCBs inhibit calcium movement leading to smooth muscle relaxation and decreased cardiac workload.
Categorization of CCBs into Phenyl Alkylamine, Benzothiazepine, and Dihydropyridines.
Comparative study of DHPs and non-DHPs in their mechanisms and effects.
Mechanisms of CCBs: decreased myocardial contraction, HR, and conduction, and vascular relaxation.
Discussion on selective action of CCBs on cardiovascular tissues.
Role of L-type Ca2+ channels in cardiac and vascular smooth muscle contraction.
Understanding differential effects CCBs have on cardiovascular cells.
Impacts of CCBs on hemodynamics.
Overview on pharmacokinetics pertinent to various CCBs.
Indications for CCBs in hypertension, angina, arrhythmias, and other conditions.
Common adverse effects associated with CCBs including specific side effects for each.
Comparison on the adverse effects among different CCBs.
Brief overview of contraindications concerning CCB usage.
Dosage recommendations and notable features for different CCBs.
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calcium channel blocker
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- 2. • Verapamil wasdeveloped in Germany in 1962 as a coronary dilator. • It had additional cardiodepressant property, but its mechanism of action was not known. • Three important classes of calcium channel blockers are examplified by: • Verapamil—a phenyl alkylamine, hydrophilic papaverine congener. • Nifedipine—a dihydropyridine (lipophilic). • Diltiazem—a hydrophilic benzothiazepine. • The dihydropyridines (DHPs) are the most potent Ca2+ channel blockers, and this subclass has proliferated exceptionally
- 3. Calcium channels • Voltagesensitive channel: Activated when membrane potential drops to around –40 mV or lower. • Receptor operated channel: Activated by Adr and other agonists— independent of membrane depolarization (NA contracts even depolarized aortic smooth muscle by promoting influx of Ca2+ through this channel and releasing Ca2+ from sarcoplasmic reticulum). • Leak channel: Small amounts of Ca2+ leak into the resting cell and are pumped out by Ca2+ATPase. Mechanical stretch promotes inward movement of Ca2+, through the leak channel or through separate stretch sensitive channel.
- 5. • DHPs arethe most commonly used calcium channel blockers (CCBs). • The cardiac and smooth muscles cell contraction depends upon the activation of calcium channels in the cardiac myocytes. For depolarization of cardiac and other smooth muscles cells, entry of calcium into the cells occurs through these calcium channels. • CCBs inhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell contraction.
- 6. • A lossof smooth muscle tone, vasodilation, and decreased peripheral resistance occurs. Subsequently, preload and afterload are decreased, which in turn decreases cardiac workload and oxygen consumption. • Short acting DHPs like nifedipine causes reflex tachycardia and palpitations, which can be controlled and minimized by addition of a beta-blocker or giving sustained release preparations.
- 7. CCB • Phenyl alkylamine: •Verapamil • Benzothiazepine: • Diltiazem • Dihydropyridines: • Nifedipine, Felodipine, Amlodipine, Nitrendipine, Nimodipine, Lacidipine, Lercanidipine, Benidipine
- 8. Comparative action ofCCBs (DHPs & non-DHPs)
- 10. MECHANISM OF ACTIONOF CCBs Decrease myocardial contraction, HR & conduction velocity Causes vacular smooth muscle relaxation Decrease calcium entry into the cardiac & smooth muscle cells Block L-type Calcium channels CALCIUM CHANNEL BLOCKERS
- 11. Why Do CCBsAct Selectively on Cardiac and Vascular Muscle?
- 12. N-type and P-typeCa2+ channels mediate neurotransmitter release in neurons
- 13. Skeletal muscle relieson intracellular Ca2+ for contraction
- 14. Cardiac cells relyon L-type Ca2+ channels for contraction and for the upstroke of the AP in slow response cells
- 15. Vascular smooth musclerelies on Ca2+ influx through L-type Ca2+ channels for contraction
- 16. CCBs Act Selectivelyon Cardiovascular Tissues • Neurons rely on N-and P-type Ca2+ channels • Skeletal muscle relies primarily on [Ca] • Cardiac muscle requires Ca2+ influx through L-type Ca2+ channels • contraction (fast response cells) • upstroke of AP (slow response cells) • Vascular smooth muscle requires Ca2+ influx through L-type Ca2+ channels for contraction
- 17. Differential effects ofdifferent CCBs on CV cells
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- 20. THERAPEUTIC USES OFCCBs • Hypertension: Long acting CCBs are used for the long term treatment of hypertension. Amlodipine is the most preferred drug. • Ischemic heart disease: • Angina pectoris: DHPs like amlodopine with beta-blocker are used for long term management. Verapamil and diltiazem are used for prophylaxis. • Vasospastic angina: Verapamil and amlodopine are the preffered agents. • Unstable angina: Verapamil is used.
- 21. • Supraventricular arrhythmia:verapamil & diltiazem are used due to their antiarrythmic properties. • Peripheral vascular disease: Nifedipine, felodipine and diltiazem are used for this purpose. Nifedipine patches are also useful. • Migraine prophylaxis: verapamil is useful. • Nocturnal leg cramps: verapamil is useful.
- 22. ADVERSE EFFECTS • Verapamilcauses Nausea, constipation, bradycardia, aggravation of • conduction defects . • Ditiazem also has similar side effect profile but slightly to lesser extent. • DHPs show side effects like nausea, headache, drowsiness palpitation, hypotension, flushing and ankle edema. • Difficulty in micturation & worsening of gastroesophageal reflux is seen in elderly patients.
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- 25. Drug Dose Specialfeatures Nifedipine 5-20mg BD Has fast onset of action with short duration. Causes reflex tachycardia as a prominent side effects. May increase frequency of angina attack. Amlodipine 5-10mg OD Has got consistent & good oral bioavailability. Diurnal fluctuation of BP are least. s-Amlodipine is its enatiomer and equally effective at half the dose with less ankle oedema. Felodipine 5-10mg OD Has higher vascular selectivity. Nitrendipine 5-20mg OD Has only 10-30% of bioavailabilty. Additionally also releases nitric oxide from the endothelium Useful in hypertension with angina. Nimodipine 30-60mg QID It is cerebrovascular selective due to high lipid solubility & BBB penetration. Used in patients with hemorrhagic stroke & subarachnoid hemorrhage. Lacidipine 4-6mg OD Has vasoselective activity and useful in hypertension only. Lercanidipine 10-20mg OD Long acting DHP. Useful in hypertension. Benidipine 4-8mg OD Long acting DHP. Has very slow dissociation from DHP receptors. Useful in hypertension & angina.