A nursing student asks how nonsteroidal anti-inflammatory drugs (NSAIDs) work to suppress inflammation and reduce pain. The nurse will explain that NSAIDs

A) Beta 1-receptors:
Beta 1-receptors are primarily found in the heart, and their stimulation leads to increased heart rate and contractility. These receptors are not typically involved in vasoconstriction, pupil dilation, or piloerection.

B) Beta 2-receptors:
Beta 2-receptors are primarily located in smooth muscles such as the bronchi and blood vessels. Their stimulation causes smooth muscle relaxation, leading to bronchodilation and vasodilation. Beta 2-receptors are not responsible for the effects of vasoconstriction, piloerection, or pupil dilation described in the question, making this option incorrect.

C) Alpha 2-receptors:
Alpha 2-receptors are involved in the inhibition of norepinephrine release and play a role in regulating sympathetic tone. They are not primarily responsible for vasoconstriction or the other physiological responses listed in the question. Alpha 2-stimulation typically results in decreased sympathetic activity, not the effects described here.

D) Alpha 1-receptors:
Alpha 1-receptors are located on smooth muscle, including the blood vessels, and their stimulation results in vasoconstriction. They are also involved in other actions such as piloerection (hair standing on end), pupil dilation (mydriasis), and closure of the salivary sphincter. Additionally, they play a role in male sexual emission (ejaculation). The physiological responses described in the question—vasoconstriction, piloerection, pupil dilation, and male sexual emission—are all consistent with alpha 1-receptor stimulation.

A) They increase norepinephrine at the neuromuscular junction: Anticholinergic agents do not directly increase norepinephrine at the neuromuscular junction. Instead, they work by blocking acetylcholine receptors (specifically muscarinic receptors) in the parasympathetic nervous system, which reduces parasympathetic activity. Norepinephrine is primarily involved in the sympathetic nervous system, not the action of anticholinergics.

B) They act to block the effects of the parasympathetic nervous system: This is the correct explanation. Anticholinergic agents work by inhibiting the action of acetylcholine at muscarinic receptors, which are part of the parasympathetic nervous system. By blocking these receptors, anticholinergics reduce parasympathetic effects such as slowing of the heart rate, increased glandular secretions, and smooth muscle contraction, leading to effects like increased heart rate, dry mouth, and bronchodilation.

C) They compete with serotonin for muscarinic acetylcholine receptor sites: Anticholinergic drugs do not interact with serotonin receptors. They specifically target muscarinic acetylcholine receptors, which are involved in parasympathetic responses. Serotonin is a different neurotransmitter, and while some drugs may affect both serotonin and acetylcholine pathways, anticholinergic agents do not compete with serotonin at these receptor sites.

D) They block nicotinic receptors: Anticholinergics typically block muscarinic receptors, not nicotinic receptors. Nicotinic receptors are involved in the transmission of signals at the neuromuscular junction and in the autonomic ganglia, while muscarinic receptors are primarily involved in parasympathetic functions. Blocking nicotinic receptors would have different effects and is not the action of anticholinergic agents.