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Questions and Answers
What is the mechanism through which nitroglycerin releases NO?
What is the mechanism through which nitroglycerin releases NO?
- Spontaneous mechanism independent of metabolism
- Enzymatic sulfhydryl group reduction (correct)
- Inhibition of protein kinase G
- Activation of guanylate cyclase
How does exogenous NO stimulate guanylate cyclase within the vascular smooth muscle cell?
How does exogenous NO stimulate guanylate cyclase within the vascular smooth muscle cell?
- By converting guanosine triphosphate to cGMP (correct)
- By increasing intracellular Ca2+ concentration
- By activating protein kinase G
- By inhibiting myosin light chains
What is the role of cGMP-dependent protein kinase (protein kinase G) in the vascular smooth muscle cell?
What is the role of cGMP-dependent protein kinase (protein kinase G) in the vascular smooth muscle cell?
- Stimulates K+ efflux from the cell
- Increases intracellular Ca2+ concentration
- Activates the sarcoplasmic reticulum Ca2+ ATPase
- Dephosphorylates myosin light chains (correct)
How does NO stimulate Ca2+ reuptake into the sarcoplasmic reticulum?
How does NO stimulate Ca2+ reuptake into the sarcoplasmic reticulum?
What effect does NO have on K+ efflux from the cell?
What effect does NO have on K+ efflux from the cell?
How does venodilation contribute to declines in LV and RV end-diastolic volume?
How does venodilation contribute to declines in LV and RV end-diastolic volume?
What effect does arterial vasodilation have on systemic and pulmonary arterial pressures?
What effect does arterial vasodilation have on systemic and pulmonary arterial pressures?
How does NO affect the sarcoplasmic reticulum Ca2+ ATPase?
How does NO affect the sarcoplasmic reticulum Ca2+ ATPase?
What is the role of cGMP in the relaxation of vascular smooth muscle?
What is the role of cGMP in the relaxation of vascular smooth muscle?
What is the primary action of nitrovasodilators in patients with heart failure?
What is the primary action of nitrovasodilators in patients with heart failure?
What effect does cellular hyperpolarization have on the voltage-gated Ca2+ channel?
What effect does cellular hyperpolarization have on the voltage-gated Ca2+ channel?
How does NO contribute to the reduction of intracellular Ca2+ concentration in vascular smooth muscle?
How does NO contribute to the reduction of intracellular Ca2+ concentration in vascular smooth muscle?
What is responsible for true tolerance to organic nitrates?
What is responsible for true tolerance to organic nitrates?
Which effect can nitroglycerin precipitate in hypovolemic patients with ischemia?
Which effect can nitroglycerin precipitate in hypovolemic patients with ischemia?
What is the primary reason for caution when using organic nitrates in patients receiving phosphodiesterase type V inhibitors?
What is the primary reason for caution when using organic nitrates in patients receiving phosphodiesterase type V inhibitors?
What is the primary cardiac effect of nitroglycerin at lower doses?
What is the primary cardiac effect of nitroglycerin at lower doses?
What is the mechanism of action of sodium nitroprusside in hypertensive emergencies?
What is the mechanism of action of sodium nitroprusside in hypertensive emergencies?
What is the primary cause of resistance to organic nitrates?
What is the primary cause of resistance to organic nitrates?
What can pseudotolerance to organic nitrates lead to after discontinuation of nitrovasodilator therapy?
What can pseudotolerance to organic nitrates lead to after discontinuation of nitrovasodilator therapy?
What is the primary effect of nitroglycerin on myocardial oxygen supply and demand?
What is the primary effect of nitroglycerin on myocardial oxygen supply and demand?
What is the effect of organic nitrates on platelet aggregation?
What is the effect of organic nitrates on platelet aggregation?
What is the primary reason for contraindicating sodium nitroprusside in acute myocardial ischemia?
What is the primary reason for contraindicating sodium nitroprusside in acute myocardial ischemia?
What effect does nitrovasodilators have on myocardial oxygen consumption?
What effect does nitrovasodilators have on myocardial oxygen consumption?
What is the mechanism through which organic nitrates may cause resistance?
What is the mechanism through which organic nitrates may cause resistance?
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Study Notes
Nitrovasodilators and Their Cardiac Effects
- Nitrovasodilators decrease myocardial oxygen consumption and increase oxygen supply through coronary artery dilation.
- Patients may display initial variability in the efficacy of nitrovasodilators, but their cardiovascular effects diminish with prolonged use.
- Resistance to organic nitrates can occur due to oxidative stress and sympathetic nervous system activation.
- Pseudotolerance may lead to rebound hypertension after discontinuation of nitrovasodilator therapy.
- Guanylate cyclase inhibition is responsible for true tolerance to organic nitrates.
- Organic nitrates may cause methemoglobinemia, interfere with platelet aggregation, and produce heparin resistance.
- Caution is advised when using organic nitrates in patients receiving phosphodiesterase type V inhibitors.
- Nitroglycerin has venodilation effects and decreases preload without a significant decrease in systemic vascular resistance at lower doses.
- Nitroglycerin improves the balance of myocardial oxygen supply and demand and is effective for myocardial ischemia.
- Nitroglycerin can precipitate life-threatening hypotension in hypovolemic patients with ischemia.
- Sodium nitroprusside is an ultra–short-acting direct NO donor and is a first-line drug for hypertensive emergencies.
- Sodium nitroprusside is contraindicated in acute myocardial ischemia due to coronary steal and pronounced reflex tachycardia.
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