L7 Flashcards
Q: How does calcium contribute to smooth muscle contraction in blood vessels?
A: Calcium binds to calmodulin, activating myosin-light chain kinase (MLCK), which phosphorylates myosin, allowing it to bind actin and cause contraction.
Q: What is the role of nitric oxide (NO) in vascular smooth muscle relaxation?
A: NO activates guanylate cyclase, which increases cGMP levels, leading to the activation of myosin phosphatase, which dephosphorylates myosin, causing relaxation.
Q: How do potassium channel activators cause vasodilation?
A: They open potassium channels, causing hyperpolarization of the membrane, which inhibits voltage-gated calcium channels and prevents smooth muscle contraction.
Q: What is the mechanism of action of ACE inhibitors like captopril?
A: ACE inhibitors block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and lowering blood pressure.
Q: Name a drug that blocks α1-adrenoceptors and its use.
A: Prazosin blocks α1-adrenoceptors, causing vasodilation, and is used to treat hypertension.
Q: How does nifedipine, a calcium channel blocker, help treat hypertension?
A: Nifedipine blocks voltage-gated calcium channels, reducing calcium entry into smooth muscle cells, which lowers the probability of contraction and causes vasodilation.
Q: What effect does angiotensin II have on blood vessels?
A: Angiotensin II binds to AT1 receptors, activating phospholipase C (PLC), increasing IP3, and raising intracellular calcium, leading to smooth muscle contraction and vasoconstriction.
Q: How does cAMP cause smooth muscle relaxation?
A: cAMP inhibits MLCK, preventing myosin phosphorylation, leading to smooth muscle relaxation.
Q: What are the side effects of industrial nitrates on the vascular system?
A: Industrial nitrates increase cGMP, causing vasodilation, but side effects include headaches and dizziness. Prolonged exposure may lead to tolerance and sudden withdrawal can trigger vasoconstriction.
Q: How does Losartan, an AT1 receptor antagonist, affect vascular tone?
A: Losartan blocks AT1 receptors, reducing IP3 production, leading to decreased calcium levels in smooth muscle and vasodilation.
Q: Explain the mechanisms through which calcium causes smooth muscle contraction and how this process can be reversed.
A: Calcium binds to calmodulin, activating myosin-light chain kinase (MLCK), which phosphorylates myosin, allowing it to bind to actin, leading to contraction. This process is reversed by increasing cAMP or cGMP, which activate protein kinases that either inhibit MLCK or activate myosin phosphatase, dephosphorylating myosin and causing relaxation.
Q: Describe the role of endothelial cells in regulating vascular tone, highlighting the effects of nitric oxide (NO) and angiotensin II.
A: Endothelial cells release NO, which activates guanylate cyclase in smooth muscle, increasing cGMP and leading to relaxation. They also release angiotensin II, which binds to AT1 receptors on smooth muscle, activating PLC, increasing IP3, and raising intracellular calcium levels, causing contraction.
Q: What are the different categories of vasodilator drugs, and how do they exert their effects?
A: Vasodilators include:
ACE inhibitors (e.g., captopril) block the conversion of angiotensin I to II.
Nitrates (e.g., glyceryl trinitrate) increase cGMP like NO.
Calcium channel blockers (e.g., nifedipine) block voltage-gated calcium channels.
Potassium channel activators (e.g., cromakalim) cause hyperpolarization.
AT1 receptor antagonists (e.g., losartan) block angiotensin II effects.
Q: How do toxicants like nitrates and lead affect the vascular system and blood cells?
A: Industrial nitrates increase cGMP, causing vasodilation but may lead to headaches, dizziness, and tolerance. Lead inhibits ALA-D, a key enzyme in heme production, affecting oxygen transport in the blood. Chloramphenicol and benzene can damage bone marrow, leading to aplastic anemia
Q: Compare and contrast the roles of cAMP and cGMP in smooth muscle relaxation. Provide examples of drugs that influence these pathways.
A: cAMP inhibits MLCK, preventing myosin phosphorylation, leading to smooth muscle relaxation. Drugs like β2-adrenoceptor agonists increase cAMP. cGMP activates myosin phosphatase, dephosphorylating myosin and also causing relaxation. Nitrates increase cGMP through NO production. Both cAMP and cGMP lower intracellular calcium, promoting vasodilation.
