Antihistamines Flashcards
Major mediator of immediate allergic and inflammatory processes
Histamine
Histamine is a significant regulator of
Gastric acid secretion
Important neurotransmitter in the central nervous system
Histamine
In the skin, mucous membranes, lungs, blood vessels, histamine synthesis depends on
Mast cells
In circulating blood, histamine synthesis depends on
Basophils
In the gastric mucosa and stomach, histamine synthesis depends on
ECL cells
In the brain, histamine synthesis depends on
Histaminergic neurons
Histamine is sequestered and bound in cytoplasmic granules of
Mast cells and basophils
Histamine is produced and stored in the gastric mucosa in the vesicles of
ECL cells
Histamine is produced and stored in the CNS in the vesicles of the
Histaminergic neurons
Antigens/allergens bind to IgE antibodies on the surface of pre-sensitized
Mast cells and basophils
This causes the aggregation of high-affinity IgE receptors, thus triggering
Degranulation
Can affect rapid degranulation and the local release of histamine
Mast cell injury/damage
Endocrine stimulation of the ECL cells or neuronal stimulation of histaminergic neurons can trigger
Rapid histamine exocytosis
Many compounds can stimulate the release of histamines from mast cells directly, without prior
Sensitization
These molecules are typically
-Can displace histamine from cytoplasmic granules
Organic bases or basic peptides
IgE-mediated histamine release is a
Type I hypersensitivity response
In activated mast cells, re-exposure to the antigen/allergen causes the bound IgE receptors to
Cross-link
Histamine receptors resulting in the inhibition of adenylyl cyclases and a decrease in cAMP
H3 and H4
Histamine receptor resulting in increased IP3 and increased DAG
H1
Histamine receptor that causes activation of adenylylcyclases and increased cAMP
H2
Leads to induced depolarization of afferent nerve endings, leading to the sensation of itch and pain
Histamine stimulation of H1
Histamine serves as a neurotransmitter for histaminergic neurons by binding
H1, H2, and H3
Histamine functions in appetite suppression and satiety by binding
H1 and H3
Histamine functions in increased wakefulness by binding
H1 and H3
Histamine functions in modulation of neurotransmitter release by binding
H3
Histamine causes dilation of terminal arterioles, postcapillary venules and pre-capillary sphincters by binding H1 and causing vascular endothelial production of
Nitric Oxide (NO)
Histamine causes dilation of terminal arterioles, postcapillary venules and pre-capillary sphincters by binding H2, leading to
VSM cAMP production and relaxation
Histamine causes contraction of endothelial cells via
H1
Histamine stimulation of H1 permits the escape of fluid, plasma proteins, and immune cells from post-capillary venules, thereby causing
Edema and decreased local BP
In some vascular beds, caused constriction of veins, further promoting edema by binding H1
Histamine
In the heart, Histamine-mediated vasodilation and decreased systemic BP leads to the indirect affect of
Reflex tachycardia
A direct effect of histamine on the cardiovascular system is minor increases in the force and rate of cardiac contraction via
H2
Engorges local micro- vasculature with blood and allows immune cells access to the injury where they can begin to remove and repair damaged cells and begin to fight infection
Histamine-mediated vasodilation
Histamine (and other released cytokines) have chemotactic properties that facilitate
Leukocyte recruitment
Histamine action on local afferent axons allows for sensation of
Foreign object