الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
The reasons for allergenic diseases have been principally connected with excessive release of histamine, from its biogenic stores, into blood circulation. Histaminergic receptors were proved to be classified into three subclasses; namely H1, H2, H3 receptor sites, in accordance to the particular biological response. The H1 agonism was shown to be responsible for initiation of the wheal and flare components in urticaria as well as in anaphylaxis, besides the production of the nociceptiveinflammatory effects. Potentiation of H2-receptors have been proved to be related to gastric acid secretion which when being at elevated levels
might lead to gastric and / or duodenal ulcers. The H3-receptors were established as presynaptic autoreceptors that could affect the release and biosynthesis of histamine.
The inconveniences behind excessive stimulation of H1-receptors were manifestable in certain symptoms including headache, nasal congestion, bronchospasm, contraction of smooth muscles, vasodilation, flushing, increased vascular permeability, hypotension and tachycardia. Before 1980’s, the alleviation of these symptoms was dependent on the administration of available classic first generation H1-antagonists. A serious disadvantage of such agents was the sedative effect, which could lead to fatigue, drowsiness, diminished alertness and impairment in cognitive function. This might be attributed to increased liposolubility that could lead to crossing of the blood-brain barriers with consequence occupation of cerebral H1-receptors. This problem was put into consideration in several research projects which led to the introduction of the non-sedating H1-antagonists, as second generation antiallergics, such as: terfenadine, cetirizine, astemazole, loratadine and acrivastine.