Pharmacology: Adrenoceptors and Their Actions

A type of adrenoceptor found in vascular smooth muscle, skin, renal, and splanchnic GIT sphincters, bladder sphincter, and radial muscle of the iris. It activates the inositol triphosphate (IP3) pathway leading to an increase in intracellular calcium (Ca++) levels.

A type of adrenoceptor found in the GIT wall and presynaptic adrenergic neurons. It inhibits adenylyl cyclase, leading to a decrease in cyclic adenosine monophosphate (cAMP) levels.

α1 adrenoceptors activate the inositol triphosphate (IP3) pathway, which triggers the release of calcium from intracellular stores. This increase in intracellular calcium leads to various cellular responses, including muscle contraction and smooth muscle vasoconstriction.

α2 adrenoceptors inhibit adenylyl cyclase, an enzyme involved in the production of cAMP. This decrease in cAMP levels reduces the activity of various cellular processes, including neurotransmitter release and smooth muscle relaxation.

α1 adrenoceptors are found in various tissues, including vascular smooth muscle, skin, renal, and splanchnic GIT sphincters, bladder sphincter, and radial muscle of the iris. These tissues play crucial roles in regulating blood pressure, blood flow, and muscle contraction.

Drugs that block the action of acetylcholine at muscarinic receptors. This can lead to a variety of effects, including decreased muscle contractions, reduced secretions, and increased heart rate.

A muscarinic blocker used to treat the tremors and rigidity associated with Parkinson's disease.

A muscarinic blocker commonly used to treat overactive bladder by reducing bladder muscle spasms.

A potent muscarinic blocker with a wide range of applications, such as treating spastic disorders of the GI tract, organophosphate poisoning, bradycardia, and suppressing respiratory secretions.

A muscarinic blocker used primarily to prevent motion sickness by suppressing signals from the inner ear to the brain.

Substances that affect the cholinergic system by influencing the actions of acetylcholine (ACh) - a neurotransmitter responsible for nerve impulse transmission.

Drugs that mimic the effects of acetylcholine (ACh) by binding to cholinoceptors, either muscarinic (M) or nicotinic (N).

Cholinergic agonists that bind directly to cholinoceptors (M or N) and mimic the actions of ACh. Their effects last longer than ACh.

Naturally occurring compounds that are esters of choline. Examples include acetylcholine (ACh) and synthetic choline esters like carbachol and bethanechol.

Chemicals found in plants that have physiological effects. Examples include nicotine and pilocarpine.

Cholinergic agonists that primarily act on muscarinic receptors (M) in the body.

Cholinergic agonists that primarily act on nicotinic receptors (N) in the body.

Receptors on the surface of cells that bind to acetylcholine (ACh). These receptors can be either muscarinic (M) or nicotinic (N).

Receptors that are directly linked to ion channels. When a neurotransmitter binds to an ionotropic receptor, it causes the channel to open or close, allowing ions to flow across the cell membrane.

A type of G protein that is coupled to α1 adrenoreceptors. When activated by norepinephrine binding to the α1 receptor, Gq protein triggers a cascade of events involving phospholipase C.

An enzyme that is activated by Gq protein. It breaks down phospholipids in the cell membrane, producing signaling molecules like diacylglycerol (DAG) and inositol triphosphate (IP3).

A signaling molecule produced by the breakdown of phospholipids. DAG activates protein kinase C, which leads to various cellular responses.

A signaling molecule produced by the breakdown of phospholipids. IP3 binds to receptors on the endoplasmic reticulum, triggering the release of calcium ions.

These essential ions play a vital role in many cellular processes, including muscle contraction, and are released from intracellular stores by IP3.

The process starts with norepinephrine binding to the α1 receptor, causing a conformational change. This activates Gq protein, which then activates phospholipase C. The breakdown of phospholipids leads to the production of DAG and IP3, which further activate protein kinase C and trigger calcium release, respectively.

Miosis is the constriction of the pupil of the eye. It is caused by the contraction of the sphincter pupillae muscle.

Cholinesterase inhibitors block the enzyme acetylcholinesterase, which breaks down acetylcholine. This increases the amount of acetylcholine at the synapse, amplifying the effect of the neurotransmitter.

Cholinergic antagonists are drugs that block the effects of acetylcholine by binding to cholinergic receptors (muscarinic or nicotinic), preventing acetylcholine from acting.

Pralidoxime reactivates the enzyme acetylcholinesterase that has been inhibited by organophosphate poisoning.

Pralidoxime cannot penetrate the central nervous system. Therefore, it is not effective in treating CNS effects of organophosphate poisoning.

Atropine is the common antidote for toxicity caused by anticholinesterase agents.

Atropine treats side effects like increased bronchial and salivary secretion, bronchoconstriction, and bradycardia (slow heart rate) caused by anticholinesterase agents.

Diazepam helps reduce persistent convulsions caused by organophosphate poisoning.

Receptors that bind to adrenaline or noradrenaline (catecholamines), triggering various physiological effects. Subtypes include β1, β2, and β3, with varying affinities for different agonists.

A potent agonist for β-adrenoreceptors, particularly β1 and β2, leading to stronger effects on the heart and lungs compared to adrenaline or noradrenaline.

A group of neurotransmitters and hormones, including adrenaline (epinephrine), noradrenaline (norepinephrine), dopamine, and isoproterenol, that bind to adrenergic receptors and trigger a cascade of physiological responses.

A class of drugs that mimic the actions of the sympathetic nervous system, activating adrenergic receptors and producing effects such as increased heart rate, vasoconstriction, and bronchodilation.

An enzyme that plays a crucial role in the inactivation of catecholamines, particularly adrenaline and noradrenaline, by adding a methyl group to their structure.

An enzyme vital for the breakdown of neurotransmitters, including catecholamines, dopamine, and serotonin, by removing their amino group.

Drugs that directly activate adrenergic receptors, producing effects by binding to and stimulating them, similar to the action of natural neurotransmitters like adrenaline and noradrenaline.

Drugs that exert their effect indirectly by increasing the concentration of neurotransmitters, such as noradrenaline, in the synaptic cleft, amplifying their signal.