Questions and Answers
What is the main reason why catecholamines administered orally are ineffective?
Which characteristic of noncatecholamines allows them to have longer half-lives compared to catecholamines?
At low doses, which adrenergic agonist acts primarily on B2 receptors only?
What is the main adverse effect of alpha-1 receptor activation?
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What is the clinical significance of activation of alpha-2 receptors in the central nervous system?
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What is the primary therapeutic application of B1 agonists?
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What is a potential adverse effect of B2 receptor activation in the uterus?
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What effect does activation of dopamine receptors have on renal vasculature?
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What is the primary reason why albuterol is considered highly selective when acting at low doses?
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Which receptor activation leads to relief of severe pain?
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What is the primary therapeutic application for activation of B2 receptors in the uterus?
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What can overstimulation of B1 receptors lead to in some cases?
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Which type of adrenergic agonists work by promotion of norepinephrine release, blockade of norepinephrine reuptake, and inhibition of norepinephrine inactivation?
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What is the main difference between catecholamines and noncatecholamines?
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Why are catecholamines unable to cross the blood-brain barrier?
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Which enzyme quickly metabolizes catecholamines?
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What is the defining feature of indirect adrenergic agonists?
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What is the chemical structure that characterizes catecholamines?
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Why do catecholamines have a brief duration of action?
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Which class of adrenergic agonists includes dopamine, epinephrine, isoproterenol, and ephedrine?
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What do noncatecholamines have in common?
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What is the main difference between direct and indirect adrenergic receptor activation?
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What property prevents chatecholamines from being used orally?
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Why are chatecholamines unable to act in the central nervous system?
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