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Adrenergic Neurons: Neurotransmission

Adrenergic Neurons: Neurotransmission

Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
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Adrenergic Receptors (Adrenoceptors): Classification

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Adrenergic receptors, or adrenoceptors, respond to the autonomic neurotransmitter noradrenaline and other endogenous catecholamine agonists. They are classified into two main families, α and β, based on their pharmacological response and are further subdivided depending on their location, elicited response, and affinity to specific agonists or antagonists.
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...

Adrenergic Receptors: ɑ Subtype

Adrenergic Receptors: ɑ Subtype

Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
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α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
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Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
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Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and anaphylaxis:...

Allergic Reactions: Anaphylaxis

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Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...

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Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

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Catecholamine responses to histamine infusion in man.

R R Schellenberg¹, H Ohtaka, H B Paddon

¹University of British Columbia Pulmonary Research Laboratory, Vancouver, Canada.

The Journal of Allergy and Clinical Immunology

|February 1, 1991

Summary

Histamine infusion significantly increases plasma norepinephrine levels, primarily through neural release, unlike nitroglycerin. This suggests neural norepinephrine plays a key role in histamine

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Area of Science:

Cardiovascular Physiology
Neuropharmacology

Background:

Histamine is known to affect blood pressure and heart rate.
The precise mechanisms of histamine's cardiovascular effects, particularly regarding catecholamine release, require further elucidation.

Purpose of the Study:

To compare the effects of histamine and nitroglycerin on plasma catecholamine levels during induced hypotension.
To investigate the source of catecholamine release (neural vs. adrenal) in response to histamine.

Main Methods:

Eight healthy men underwent incremental histamine infusions in a 30-degree tilt position, monitoring blood pressure and heart rate.
Plasma catecholamine (norepinephrine and epinephrine) levels were measured during histamine infusion and compared to measurements during nitroglycerin-induced hypotension.
Dose escalation continued until mean blood pressure decreased by >15 mm Hg or a maximum histamine dose was reached.

Main Results:

Histamine caused significantly greater increases in heart rate and plasma norepinephrine (NE) compared to nitroglycerin for similar blood pressure reductions.
Histamine infusion led to a two- to fivefold increase in NE levels, with minimal changes in epinephrine.
Data indicate selective NE release from adrenergic nerve terminals, with limited adrenal catecholamine involvement.

Conclusions:

Histamine selectively stimulates norepinephrine release from sympathetic nerve endings.
Neural norepinephrine release is a significant contributor to the cardiac effects observed during histamine administration.
This finding clarifies the role of the sympathetic nervous system in mediating histamine's cardiovascular actions.