Pharmacological characterization of histamine receptors in the mouse seminal vesicle: Sensitivity to H₁- and H₂-receptor agonists and antagonists

Neither histamine nor the more specific H₁- or H₂-receptor agonists (0.2-220 μM) produced a contraction of the mouse seminal vesicle. However, all these agonists decreased resting tone and caused a dose-related inhibition of the electrically evoked twitch responses in these concentrations. The slopes of the percentage response versus log molar concentration curves for all agonists did not differ significantly from that of histamine. The rank order and relative potency of the compounds tested were: histamine (100%)>dimaprit (65%)≧4-methylhistamine (36%)>2-methylhistamine (4.5%)>2-(2-thiazolyl) ethylamine (1.7%). Inhibition of the twitch response by histamine was antagonized by cimetidine (3.5-140 μM) but not by mepyramine (0.1-1.0 μM). The slopes of Schild plots for cimetidine against histamine and dimaprit did not differ from unity, and the calculated pA₂ values of cimetidine were 5.70 and 5.55, respectively. Histamine (2.2 and 6.5 μM) inhibited the contraction elicited by a submaximal concentration of exogenous noradrenaline (1 μM); this inhibition could also be selectively antagonized by cimetidine. These results demonstrate that histamine and selective H₁- and H₂-receptor agonists have an inhibitory action on the mouse seminal vesicle, and that this action is mediated via a post-junctional H₂-receptor. The calculated pA₂ values of cimetidine against histamine and dimaprit also suggest that the receptor in the mouse seminal vesicle is of the conventional H₂-type. The results further indicate that an H₁-receptor is absent in the mouse seminal vesicle.