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Abstract
The role of histamine H1- and H2-receptors in mediating the response produced by histamine was investigated on rat ocular surface. Histamine caused a dose-dependent increase in microvascular permeability on this surface. Response to histamine was significantly inhibited by pretreatment with chlorpheniramine (an H1-antagonist) but was unchanged by cimetidine (an H2-antagonist). No additive effect was shown when chlorpheniramine and cimetidine were used in combination. Moreover, dimaprit, a selective histamine H2-receptor agonist, failed to elicit a dose-dependent vasopermeability response. Chlorpheniramine significantly reduced increase in microvascular permeability associated with immediate hypersensitivity, although cimetidine did not. The addition of cimetidine to chlorpheniramine did not lead to greater reduction than that achieved with chlorpheniramine alone. We conclude that the microvascular permeability response to histamine is predominantly mediated by H1-receptors on rat ocular surface.
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