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 H-1 receptor antagonist), cimetidine (a histamine H-2 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 H-1 and H-2 receptors (2) in simian but not in canine arteries, there exist histamine H-3 receptors, although their role is not clear (3) histamine induces a vasoconstriction mediated via histamine H-1 receptors and a vasodilatation via H-2 receptors which exist in vascular smooth muscle, and (4) in simian but not in canine arteries, there are endothelium-dependent vasodilatation mechanisms.