L8 Flashcards
How is the resting membrane potential of cardiac muscle cells maintained?
The Na+/K+ ATPase pump maintains the resting membrane potential by pumping Na⁺ out of and K⁺ into the cell.
What triggers cardiac muscle contraction at the cellular level?
An action potential opens L-type Ca²⁺ channels, causing Ca²⁺ influx. This triggers ryanodine receptors in the sarcoplasmic reticulum (SR) to release more Ca²⁺, which binds to troponin, enabling actin-myosin interaction and contraction.
What is the mechanism of action of β1-adrenoceptor agonists like dobutamine?
β1-adrenoceptor agonists activate adenylate cyclase (AC), increasing cAMP, which enhances heart rate and contraction force. Dobutamine is used to treat cardiogenic shock.
How do calcium channel blockers like verapamil affect the heart?
Calcium channel blockers inhibit L-type Ca²⁺ channels, reducing calcium influx, which decreases heart rate and contractility. They are used for tachycardias, angina, and hypertension.
What is the role of digoxin in treating heart conditions?
Digoxin inhibits the Na+/K+ ATPase, increasing intracellular Na⁺ and Ca²⁺ levels, enhancing cardiac contractility. It is used in heart failure.
What are the effects of sodium channel blockers like lidocaine on cardiac function?
Sodium channel blockers decrease the probability of action potential generation, delaying contraction and stabilizing arrhythmias.
How do organic nitrates like nitroglycerin alleviate angina?
Organic nitrates release nitric oxide (NO), which activates guanylate cyclase in smooth muscle, increasing cGMP and causing vasodilation.
What toxicants are known to induce cardiomyopathy, and how?
Cobalt: Blocks calcium channels.
Ethanol: Degenerates myocytes and proteins over time.
Doxorubicin: Metabolized into free radicals, damaging DNA and mitochondria.
How do toxins like tetrodotoxin and saxitoxin affect cardiac function?
They block sodium channels, reducing the likelihood of action potential initiation and delaying contraction.
What is cardiomyopathy, and how does it affect the heart?
Cardiomyopathy is progressive damage to cardiac muscle, reducing contractility and potentially leading to heart failure.
Explain the process of cardiac muscle contraction and how it is regulated by calcium.
Cardiac contraction begins with an action potential opening L-type Ca²⁺ channels, allowing Ca²⁺ influx. This triggers ryanodine receptors in the SR to release stored Ca²⁺, amplifying the signal. Ca²⁺ binds to troponin, inhibiting its function and enabling actin-myosin interaction for contraction. Relaxation occurs when Ca²⁺ is pumped back into the SR by SERCA.
Compare the mechanisms and clinical uses of β1-adrenoceptor agonists and antagonists.
Agonists (e.g., dobutamine) activate β1 receptors, increasing cAMP and enhancing heart rate and contraction. Used in cardiogenic shock.
Antagonists (e.g., metoprolol) block β1 receptors, reducing cAMP, lowering heart rate, and decreasing oxygen demand. Used in angina, hypertension, and arrhythmias.
Describe the toxic effects of digoxin and how they affect cardiac function.
Digoxin inhibits the Na+/K+ ATPase, increasing intracellular Na⁺, which indirectly raises Ca²⁺ levels via the Na+/Ca²⁺ exchanger. Excessive levels can cause ectopic beats, arrhythmias, and toxicity by disrupting electrical conduction.
Discuss the role of calcium channel blockers in cardiac therapy and provide examples.
Calcium channel blockers (e.g., verapamil, nifedipine) inhibit L-type calcium channels, reducing Ca²⁺ influx into cardiac and smooth muscle cells. This decreases contractility, slows the heart rate, and reduces vascular resistance. They are used for tachycardia, angina, and hypertension.
How do toxicants like ethanol and doxorubicin contribute to cardiomyopathy?
Ethanol causes chronic degeneration of myocytes and proteins, impairing contractility.
Doxorubicin generates free radicals that damage DNA and mitochondria, leading to apoptosis and decreased cardiac function. Both lead to congestive heart failure over time.
