Regional vascular resistance and heart rate responses mediated through H1- and H2-histamine receptors in the unanaesthetised rabbit.

The effects of histamine infusions (10-100 microgram/kg/min) on heart rate and hindlimb, carotid, mesenteric and renal vascular resistance were investigated in unanaesthetised rabbits after "total" autonomic effector block to abolish reflex effects. Histamine caused a rise in heart rate that was predominately due to stimulation of H2-receptors (blocked by metiamide). Hindlimb and carotid vascular resistance did not change significantly during histamine infusion. However, after blocking H2-receptors with metiamide histamine infusions produced dose-related vasoconstriction in these beds while after H1-receptor block with mepyramine histamine caused dose-related vasodilatation indicating that H1- and H2-RECEPTORS MEDIATED OPPOSITE VASCULAR EFFECTS WHICH WERE OF SIMILAR MAGNITUDE. By contrast, histamine infusion caused vasodilatation in both the mesenteric and renal vasculature before giving antagonists. This dilatation was mediated by both H1- and H2-RECEPTORS AS EITHER RECEPTOR ANTAGONIST ATTENUATED THE RESPONSE. These studies suggest that H1-receptors in the same species mediate vasoconstriction in som- beds and vasodilatation in others while H2-receptors mediate vasodilatation in all the beds studied and also account for most of the increase in heart rate.