Neither histamine nor the more specific H1- or H2-receptor agonists (0.2-220 micrometers) 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%) greater than dimaprit (65%) greater than 4-methylhistamine (36%) greater than 2-methylhistamine (4.5%) greater than 2-(2-thiazolyl) ethylamine (1.7%). Inhibition of the twitch response by histamine was antagonized by cimetidine (3.5-140 micrometers) but not by mepyramine (0.1-1.0 micrometer). 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 micrometers) inhibited the contraction elicited by a submaximal concentration of exogenous noradrenaline (1 micrometer); 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 of the conventional H1-type. The results further indicate that an H1-receptor is absent in the mouse seminal vesicle.
Animals Cimetidine