PHARMACOLOGICAL ANALYSIS OF HISTAMINE RECEPTORS IN MUSCULATURE AND VASCULATURE OF THE DOG TRACHEA in situ

Abstract

1 The role of histamine H1-and H2-receptors in the musculature and vasculature of the dog trachea was investigated in the blood-perfused trachea in situ. 2 Histamine and acetylcholine caused increases in blood flow (tracheal vasodilatation) and in intraluminal pressure (tracheal constriction) in a dose-dependent manner. Histamine was almost equipotent to acetylcholine in causing tracheal vasodilatation but was about 30 times less potent in causing tracheal constriction. 3 The histamine H2-receptor agonist, dimaprit, caused a dose-dependent increase in tracheal blood flow but failed to cause tracheal constriction. 4 The tracheal constriction produced by histamine was inhibited strongly by diphenhydramine but not modified by metiamide. The tracheal vasodilatation produced by histamine was antagonized by both diphenhydramine and metiamide; diphenhydramine was more effective than metiamide. 5 It is concluded that in the tracheal musculature, histamine receptors are exclusively of the H1-type and mediate constriction, whereas in the tracheal vasculature, both histamine H1-and H2-receptors mediate vasodilatation but histamine Hl-receptors are predominant.

Characterization of neuronal and vascular histamine receptors mediating the salivary and vasodilator responses to histamine of the dog submandibular gland.

“…In the presence of mepyramine the dose-response curves for the early blood flow response to dimaprit and histamine were also parallel, but dimaprit was about 750 times less potent than histamine in producing the early blood flow response on a molar basis. Dimaprit has been reported to be about 5 times less potent than histamine in increasing blood flow through the hind limb of the cat (Parsons et al 1977), whereas in the tracheal vascular bed of the dog it has been shown to be about 100 times less potent than histamine in producing vasodilatation (Himori and Taira 1978). Thus, it appears that in the glandular vascular bed histamine H1-receptors are far more predominant than the histamine H2-receptors as compared with other vascular beds.…”

Effects of histamine on neurally mediated contraction of canine tracheal smooth muscle.

“…Histamine causes airway contraction through H, -receptors; and in some species, it causes airway dilatation via H2-receptors (9). In the canine airway, however, histamine receptors are exclusively of the H, -type which mediate constrictions (10,11). Recently, it has been reported that H3-receptors which inhibit ACh release are present on the vagus nerve in guinea pig and human airways (12,13).…”