Responses to histamine and acetylcholine in isolated monkey mesenteric veins versus arteries

The aim was to analyse and compare mechanisms of histamine or acetylcholine action in mesenteric venous and arterial strips obtained from Japanese monkeys.

Monkey mesenteric arterial and venous strips were suspended for isometric tension recording in modified Ringer-Locke solutions, and responses of the strips precontracted with prostaglandin F2 alpha to histamine or acetylcholine were compared.

Histamine (2 x 10(-8) M-10(-5) M) produced a concentration related relaxation in the arteries and veins. The arterial relaxation was slightly but significantly attenuated by endothelial denudation [57.1(SEM 11.2)% inhibition at 10(-7) M, n = 14, p < 0.05] and treatment with 10(-6) M chlorpheniramine [26.7(6.7)% inhibition at 10(-7) M, n = 10, p < 0.05] or 10(-5) M methylene blue [31.5(11.2)% inhibition at 10(-7) M, n = 9, p < 0.05], and markedly suppressed by 10(-5) M cimetidine [96.8(1.2)% inhibition at 10(-7) M, n = 13, p < 0.001]. Indomethacin (10(-6) M) was without effect. On the other hand, relaxant responses to histamine of the venous strips were not influenced by endothelial denudation and treatment with chlorpheniramine or indomethacin but were abolished by treatment with cimetidine. Removal of the endothelium did not alter the venous relaxation caused by acetylcholine (10(-8) M-10(-4) M) but almost abolished the response to Ca2+ ionophore A23187 (10(-7) M) and substance P (10(-7) M). The acetylcholine induced relaxation was reversed to a contraction by indomethacin.

Histamine-induced relaxations of monkey mesenteric arteries seem to be associated mainly with activation of the H2 receptor subtype in smooth muscle and partially mediated by relaxing factor liberated by stimulation of the H1 subtype in the endothelium, whereas the mesenteric venous relaxation seems to be due exclusively to a mediation of H2 receptors. Acetylcholine-induced relaxations of venous strips appear to be caused by vasodilator prostanoids, possibly prostaglandin I2, liberated from subendocardial tissues.