Cholinoceptor-activating & Cholinesterase-inhibiting Drugs

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| By Thames

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| Questions: 14

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1. Can you name some examples of choline esters?

GABA

Epinephrine

- Acetylcholine
- Methacoline (acetyl-beta-methylcholine)
- Carbachol (carbamoylcholine)
- Bethanechol (carbamoyl-beta-methylcholine)
(S)- is much more potent than (R)- at muscarinic receptors

Dopamine

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Cholinoceptor-activating & Cholinesterase-inhibiting Drugs - Quiz

Questions on/ Identification of Cholinoceptor-Activating & Cholinesterase-Inhibiting Drugs

2. Name some cholinomimetic Alkaloids.

1. Atropine 2. Ephedrine 3. Scopolamine

1. Pilocarpine
2. Muscarine
1 & 2 are mainly muscarinic
3. Nicotine
4. Lobeline
3 & 4 are mainly nicotinic

Atropine, Ephedrine, and Scopolamine are not cholinomimetic alkaloids as they do not mimic the actions of acetylcholine like Pilocarpine, Muscarine, Nicotine, and Lobeline do.

Explanation

Atropine, Ephedrine, and Scopolamine are not cholinomimetic alkaloids as they do not mimic the actions of acetylcholine like Pilocarpine, Muscarine, Nicotine, and Lobeline do.

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3. M1 Receptor: Where is it found, what subtype of G protein is involved, and what is the post-receptor mechanism that is involved?

1. Kidneys, 2. Gs, 3. Protein kinase A activation

1. Brain, 2. Gs/12, 3. cAMP signaling pathway

1. Muscles, 2. Gi/o, 3. Calcium channel activation

1. Nerves
2. G_q/11
3. IP3, DAG cascade

The M1 receptor is primarily found in nerves, signaling through the Gq/11 subtype of G protein and activating the IP3, DAG cascade as its post-receptor mechanism.

Explanation

The M1 receptor is primarily found in nerves, signaling through the Gq/11 subtype of G protein and activating the IP3, DAG cascade as its post-receptor mechanism.

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4. M2 Receptor: Where is it found, which subtype of G protein is involved, and what is the post-receptor mechanism?

1. Heart, Nerves, Smooth Muscle
2. G_i/o
3. Inhibition of cAMP production, activation of K+ channels

Brain, Liver, Skeletal Muscle; G_s; Activation of cAMP production, inhibition of Na+ channels

Lung, Kidney, Intestine; G_q; Activation of cGMP production, inhibition of Ca2+ channels

Skin, Pancreas, Blood Vessels; G_alpha12/13; Activation of IP3 production, inhibition of Cl- channels

The M2 receptor is primarily found in the heart, nerves, and smooth muscle. It is coupled with the G_i/o subtype of G protein and activates the inhibition of cAMP production and the activation of K+ channels.

Explanation

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5. M3 Receptor:

3. cAMP signaling pathway

1. Glands, Smooth Muscle, Endothelium
2. G_q/11
3. IP3, DAG cascade

1. Central Nervous System, Bone Marrow, Striated Muscle

2. Gs

The M3 receptor is predominantly found in glands, smooth muscle, and endothelium. The subtype of G protein involved is Gq/11, and the post-receptor mechanism includes the IP3, DAG cascade.

Explanation

The M3 receptor is predominantly found in glands, smooth muscle, and endothelium. The subtype of G protein involved is Gq/11, and the post-receptor mechanism includes the IP3, DAG cascade.

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6. M4 Receptor: Where is it found? What subtype of G protein is involved? What is the post-receptor mechanism that is involved?

1. Peripheral Nervous System / G_q/11 / Activation of cAMP production

2. Cardiovascular system / G_s / Activation of IP3 production

1. CNS
2. G_i/o
3. Inhibition of cAMP production

3. Gastrointestinal system / G_12/13 / Inhibition of Ca2+ channels

The M4 receptor is predominantly found in the central nervous system (CNS) and signals through G_i/o protein to inhibit cAMP production as the post-receptor mechanism. The incorrect answers provide alternative locations, G protein subtypes, and signaling mechanisms that are not associated with the M4 receptor.

Explanation

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7. M5 Receptor: Where is it found?

Peripheral nervous system

Muscle tissue

1. CNS
2. G_q/11
3. IP3, DAG cascade

Endocrine glands

M5 receptor is primarily found in the Central Nervous System (CNS).

Explanation

M5 receptor is primarily found in the Central Nervous System (CNS).

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8. Where is the Nicotinic Receptor of the muscle type found?

Central nervous system

Cardiac muscle cells

1. Skeletal muscle neuromuscular junction
2. pentamer [(alpha1)2_beta1_delta_ gamma]
3. Na+, K+ depolarizing ion channel

Adrenal glands

The Nicotinic Receptor of the muscle type is specifically found at the skeletal muscle neuromuscular junction.

Explanation

The Nicotinic Receptor of the muscle type is specifically found at the skeletal muscle neuromuscular junction.

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9. Nicotinic Receptor of the neuronal type: where is it found, what subtype of G protein is involved, and what is the post-receptor mechanism that is involved?

1. CNS postganglionic cell body, dendrites
2. pentamer with alpha and beta subunits only
3. Na+, K+ depolarizing ion channel

1. CNS presynaptic axon terminals 2. trimer with beta and gamma subunits only 3. Cl- hyperpolarizing ion channel

1. Cardiac muscle cells 2. monomer with alpha subunit only 3. Cl-, Ca2+ depolarizing ion channel

1. Peripheral nervous system ganglionic cell body, axon terminals 2. dimer with alpha, beta, and gamma subunits 3. Ca2+ depolarizing ion pump

Nicotinic Receptor neuronal type is primarily found in the CNS postganglionic cell body and dendrites. It consists of a pentamer with alpha and beta subunits only and is involved in the Na+, K+ depolarizing ion channel mechanism for post-receptor function.

Explanation

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10. How would you classify pilocarpine as a drug? What is the action of pilocarpine on the muscles of the iris and cilia?

1. It is a beta blocker that inhibits sympathetic activity. Dilatation of these muscles.

1. It is an alkaloid that is a cholinoceptor agonist
2. Constriction of these muscles

2. It is a corticosteroid that reduces inflammation. Relaxation of these muscles.

3. It is an antihistamine that blocks histamine receptors. Stimulation of these muscles.

Pilocarpine is classified as an alkaloid cholinoceptor agonist because it acts on cholinergic receptors, leading to constriction of the muscles of the iris and cilia. The incorrect answers provide inaccurate classifications and actions for pilocarpine.

Explanation

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11. A 62 year-old woman is noted to have open angle glaucoma. She inadvertently applies excessive pilocarpine to her eyes. This may result in which of the following?

B. Decreased GI motility

A. Bronchial smooth muscle dilation

C. Dilation of blood vesselsM
Excessive pilocarpine may initially result in dilation of blood vessels with a drop in blood pressure and a compensatory reflex stimulation of heart rate. Higher levels will directly inhibit heart rate. In addition, pilocarpine stimulation of muscarinic cholinoreceptors can result in miosis, bronchial smooth muscle constriction, and increased GI motility.

D. Mydriasis

Excessive pilocarpine may initially result in dilation of blood vessels with a drop in blood pressure and a compensatory reflex stimulation of heart rate. Higher levels will directly inhibit heart rate. In addition, pilocarpine stimulation of muscarinic cholinoreceptors can result in miosis, bronchial smooth muscle constriction, and increased GI motility.

Explanation

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12. Muscarinic cholinergic agonistsA. Activate inhibitory G proteins (G_i)B. Decrease production of IP3C. Decrease release of intracellular calciumD. Inhibit the activity of phospholipase C.

C. Decrease release of intracellular calcium

D. Inhibit the activity of phospholipase C

B. Decrease production of IP3

A. Activate inhibitory G proteins (G_i)
In addition to activating inhibitory G proteins, muscarinic cholinergic agonists stimulate the activity of phospholipase C, increase production of IP3, and increase release of intracellular calcium.

In addition to activating inhibitory G proteins, muscarinic cholinergic agonists stimulate the activity of phospholipase C, increase production of IP3, and increase release of intracellular calcium.

Explanation

In addition to activating inhibitory G proteins, muscarinic cholinergic agonists stimulate the activity of phospholipase C, increase production of IP3, and increase release of intracellular calcium.

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13. Choline esters like carbachol are most likely to cause which of the following adverse effects?

D. Tachycardia (rapid heart rate)

A. Anhydrosis (dry skin)

C. Diarrhea, salivation, and lacrimation may be seen.
Heart rate is usually slowed, and choline esters do not cross the blood brain barrier so delirium is not an adverse effect.

B. Delirium

Diarrhea, salivation, and lacrimation may be seen. Heart rate is usually slowed, and choline esters do not cross the blood brain barrier so delirium is not an adverse effect.

Explanation

Diarrhea, salivation, and lacrimation may be seen. Heart rate is usually slowed, and choline esters do not cross the blood brain barrier so delirium is not an adverse effect.

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14. Which of the following cardiac effects may be caused by the action of cholinergic agonists or by the action of acetylcholine?

A. Increased atrioventricular (AV) conduction velocity

D. Decreased atrioventricular (AV) conduction velocity

C. Negative inotropic effect
Acetylcholine is theneurotransmitter released from cholinergic or parasympathetic (vagal)nerve fibers at the heart.
Cholinergic agonists such as choline estersand anticholinesterases act as parasympathomimetics at the heart tosimulate acetylcholine's action and decrease the force of myocardialcontraction (negative inotropism).
Increased conduction velocity (ordecreased atrioventricular conduction time), as well as increasedelectrical activity throughout the heart, and at the SA node inparticular, are typical cardiac responses resulting from adrenergicstimulation or cholinergic blockade.

B. Stimulation of the sinoatrial node (SA node)

Acetylcholine is the neurotransmitter released from cholinergic or parasympathetic (vagal) nerve fibers at the heart. Cholinergic agonists such as choline esters and anticholinesterases act as parasympathomimetics at the heart to stimulate acetylcholine's action and decrease the force of myocardial contraction (negative inotropism). Increased conduction velocity (or decreased atrioventricular conduction time), as well as increased electrical activity throughout the heart, and at the SA node in particular, are typical cardiac responses resulting from adrenergic stimulation or cholinergic blockade.

Explanation

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