Info

Receptor G Protein

Intracellular Signaling

Tissue Distribution

Selective Agonists

Selective Antagonists

Hj G q/ii Phospholipase C—mediated

Ca++ mobilization

Brain, smooth muscle, heart, endothelium

2-(3-trifluoromethyl) phenyl histamine

Mepyramine, chlor-pheniramine, triplodine Cimetidine, raniti-dine, famotidine

Hj G q/ii Phospholipase C—mediated

Ca++ mobilization

H2 Gs Adenylyl cyclase-catalyzed cAMP production

H3 G i/o Decreased Ca++ influx through G protein-coupled N-type Ca++ channels

H4 G i/o Decreased Ca++ influx through G protein coupled N-type Ca++ channels

Brain, smooth muscle, heart, endothelium

Brain, stomach, smooth muscle, heart, mast cells

Brain, autonomic nerve endings, some endothelia

Bone marrow, brain, peripheral leukocytes, lung

2-(3-trifluoromethyl) phenyl histamine

Arpromidine, impro-midine, amthamine, dimaprit Imetit, immepip, R-a-methylhistamine

Mepyramine, chlor-pheniramine, triplodine Cimetidine, raniti-dine, famotidine

Thioperamide, iodophenpropit, clobenpropit and protein into the extracellular space and eventually edema. This Hi-receptor-mediated process is responsible for the urticarial effect of histamine on the skin (hives).

In addition to its effects on the vasculature, hista-mine exerts direct positive inotropic and chronotropic effects on the heart through the stimulation of H2-receptors. H3-receptors on sympathetic nerve terminals in the heart decrease norepinephrine release; however, this effect appears to be significant only during stress states such as ischemia.

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