Podcast
Questions and Answers
What is the primary role of guanylate cyclase (GC) in the context of smooth muscle relaxation?
What is the primary role of guanylate cyclase (GC) in the context of smooth muscle relaxation?
- Inhibiting the production of nitric oxide (NO) to prevent vasodilation.
- Directly blocking the action of phosphodiesterase-5 (PDE5).
- Converting GTP into cGMP, which sustains smooth muscle relaxation. (correct)
- Breaking down cGMP into GMP to promote muscle contraction.
How does phosphodiesterase-5 (PDE5) affect smooth muscle contraction?
How does phosphodiesterase-5 (PDE5) affect smooth muscle contraction?
- It increases cGMP levels, leading to prolonged vasodilation.
- It directly activates nitric oxide (NO) production, which causes vasodilation.
- It converts cGMP into GMP, reducing cGMP levels and promoting muscle contraction. (correct)
- It converts GTP into cGMP, promoting muscle relaxation.
What is the direct consequence of inhibiting PDE5 on cGMP levels and smooth muscle tone?
What is the direct consequence of inhibiting PDE5 on cGMP levels and smooth muscle tone?
- Increased cGMP levels, promoting vasodilation. (correct)
- Decreased cGMP levels, promoting vasoconstriction.
- Conversion of GMP to cGMP, which leads to vasoconstriction.
- No change in cGMP levels, maintaining the current muscle tone.
Which molecular mechanism explains how nitric oxide (NO) causes vasodilation?
Which molecular mechanism explains how nitric oxide (NO) causes vasodilation?
If a drug inhibits guanylate cyclase, what direct effect would this have on smooth muscle?
If a drug inhibits guanylate cyclase, what direct effect would this have on smooth muscle?
How do PDE5 inhibitors contribute to the treatment of erectile dysfunction?
How do PDE5 inhibitors contribute to the treatment of erectile dysfunction?
What would be the expected outcome of a mutation that causes a complete loss of PDE5 function?
What would be the expected outcome of a mutation that causes a complete loss of PDE5 function?
Why is the conversion of cGMP to GMP by PDE5 important for regulating blood flow?
Why is the conversion of cGMP to GMP by PDE5 important for regulating blood flow?
Following administration of a PDE5 inhibitor, which of the following changes would be expected in smooth muscle cells?
Following administration of a PDE5 inhibitor, which of the following changes would be expected in smooth muscle cells?
A researcher is studying the effects of a new drug on smooth muscle. They observe that the drug increases cGMP levels but does not affect guanylate cyclase or PDE5 activity. What is the most likely mechanism of action of this drug?
A researcher is studying the effects of a new drug on smooth muscle. They observe that the drug increases cGMP levels but does not affect guanylate cyclase or PDE5 activity. What is the most likely mechanism of action of this drug?
Flashcards
Guanylate Cyclase (GC)
Guanylate Cyclase (GC)
Enzyme activated by nitric oxide (NO) that converts GTP into cGMP.
Cyclic Guanosine Monophosphate (cGMP)
Cyclic Guanosine Monophosphate (cGMP)
Molecule produced by guanylate cyclase that sustains smooth muscle relaxation, leading to vasodilation.
Phosphodiesterase-5 (PDE5)
Phosphodiesterase-5 (PDE5)
Enzyme that breaks down cGMP into inactive GMP, leading to vasoconstriction.
PDE5 Inhibitors
PDE5 Inhibitors
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Vasoconstriction
Vasoconstriction
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Vasodilation
Vasodilation
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Guanosine Monophosphate (GMP)
Guanosine Monophosphate (GMP)
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Study Notes
- Nitric oxide (NO) activates guanylate cyclase (GC).
- GC converts GTP into cGMP.
- cGMP sustains smooth muscle relaxation.
- Smooth muscle relaxation causes vasodilation, especially in penile blood vessels.
- Phosphodiesterase-5 (PDE5) converts cGMP into inactive GMP.
- GMP leads to muscle contraction and vasoconstriction.
- PDE-5 inhibitors block the PDE5 enzyme.
- Blocking PDE5 prevents the conversion of cGMP into GMP.
- Higher cGMP levels prolong smooth muscle relaxation.
- Prolonged smooth muscle relaxation leads to sustained vasodilation.
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