Endothelium-dependent vasodilatation mechanisms by histamine in simian but not in canine femoral arterial branches.

1. The vascular response of isolated, perfused canine and simian femoral arteries, which distribute blood to deep skeletal muscles, were investigated. 2. The vascular responses to histamine, 2-pyridylethylamine (2-PEA), dimaprit and alpha-methylhistamine were pharmacologically analyzed in canine and simian vessels, using diphenhydramine (DPH, a histamine H1 receptor antagonist), cimetidine (a histamine H2 antagonist) and saponin which readily removed the endothelium. 3. In canine arteries, alpha-methylhistamine showed no vascular response, but in simian preparations, it caused a slight vasoconstriction. 4. In canine arteries, histamine and 2-PEA consistently induced a vasoconstriction in preconstricted and non-preconstricted preparations. However, in simian arteries histamine usually produced a vasodilatation at small doses (less than 10(-7) mol) and a vasoconstriction at large doses in preconstricted preparations. 5. Vasoconstrictor responses to histamine and 2-PEA were significantly inhibited by DPH in both species. In simian vessels, histamine- and dimaprit-induced vasodilatations were significantly inhibited by cimetidine. 6. After removal of the endothelium by intraluminal treatment with saponin in canine femoral arteries, the vascular responses to histamine, 2-PEA and dimaprit were not significantly affected. On the other hand, in simian femoral arteries, the vasodilatation responses to histamine and 2-PEA were significantly depressed by the removal of endothelium. 7. It is concluded that (1) in both simian and canine femoral arterial branches, there are abundant histamine H1 and H2 receptors (2) in simian but not in canine arteries, there exist histamine H3 receptors, although their role is not clear (3) histamine induces a vasoconstriction mediated via histamine H1 receptors and a vasodilatation via H2 receptors which exist in vascular smooth muscle, and (4) in simian but not in canine arteries, there are endothelium-dependent vasodilatation mechanisms.