Participation of H1 and H2 histamine receptors in physiological vasodilator responses.
Histamine causes vasodilation in the dog by activation of H1 and H2 receptors blocked by mepyramine and metiamide, respectively. Experiments were conducted in anesthetized dogs to determine the participation of H1 and H2 receptors in several forms of physiological dilatation. Mepyramine attenuated both histamine-induced and active-reflex dilatation in the hindlimb. Metiamide caused a further reduction in both sets of dilatation. Neither single nor combined antihistamines reduced dilatation due to exercise or after temporary occlusion of the circulation in the hindlimb. Poststimulation dilatation in the gracilis muscle was partially attenuated by metiamide or mepyramine. Neither dilatation caused by sympathetic nerve stimulation in the hindpaw nor dilatation in the gracilis muscle caused by compound 48/80 was reduced by mepyramine. Following combined H1- and H2-receptor blockade, portions of both types of dilatation were reduced. These data provide evidence for the participation of both types of histamine receptor in active reflex dilatation, low-frequency neurogenic dilatation, dilatation caused by compound 48/80, and poststimulation dilatation. Neither type of histamine receptor appears to be involved in reactive hyperemia or dilatation caused by exercise.
Participation of H1 and H2 histamine receptors in physiological vasodilator responses. Histamine causes vasodilation in the dog by activation of H1 and H2 receptors blocked by mepyramine and metiamide, respectively. Experiments were conducted in anesthetized dogs to determine the participation of H1 and H2 receptors in several forms of physiological dilatation. Mepyramine attenuated both histamine-induced and active-reflex dilatation in the hindlimb. Metiamide caused a further reduction in both sets of dilatation. Neither single nor combined antihistamines reduced dilatation due to exercise or after temporary occlusion of the circulation in the hindlimb. Poststimulation dilatation in the gracilis muscle was partially attenuated by metiamide or mepyramine. Neither dilatation caused by sympathetic nerve stimulation in the hindpaw nor dilatation in the gracilis muscle caused by compound 48/80 was reduced by mepyramine. Following combined H1- and H2-receptor blockade, portions of both types of dilatation were reduced. These data provide evidence for the participation of both types of histamine receptor in active reflex dilatation, low-frequency neurogenic dilatation, dilatation caused by compound 48/80, and poststimulation dilatation. Neither type of histamine receptor appears to be involved in reactive hyperemia or dilatation caused by exercise.