Casteels R, Suzuki H
Pflugers Arch. 1980 Aug;387(1):17-25. doi: 10.1007/BF00580839.
Histamine activates both H1- and H2-receptors in the ear artery of the rabbit. The specific action of these receptor activations on the membrane potential and the force development has been investigated by using the H1-blocking agent mepyramine and the H2-blocking agent cimetidine. H1-activation depolarizes and increases force development, while H2-activation hyperpolarizes and reduces force development. These effects on the force development can occur independently of the changes of the membrane potential. By determining the effect of histamine on tissues which were denervated with 6-hydroxydopamine it was shown that histamine exerts its effect directly on the smooth muscle cells. Na-deficiency depolarizes the smooth muscle cells, but it also reduces the changes of the membrane potential and the force development induced by H1-stimulation. K-free medium prevents the hyperpolarizing effect of H2-activation. As far as the ion fluxes are concerned an H1-activation is found to induce an increased efflux of K while a simultaneous H2-activation only reduces the increase of flux induced by H1-activation. H1-activation induces a release of Ca from the intracellular Ca stores, while H2-activation inhibits this release.
组胺可激活兔耳动脉中的H1和H2受体。通过使用H1阻断剂美吡拉敏和H2阻断剂西咪替丁，研究了这些受体激活对膜电位和力产生的具体作用。H1激活使膜电位去极化并增加力的产生，而H2激活使膜电位超极化并降低力的产生。这些对力产生的影响可独立于膜电位的变化而发生。通过测定组胺对用6-羟基多巴胺去神经支配的组织的作用，表明组胺直接作用于平滑肌细胞。缺钠使平滑肌细胞去极化，但也减少了H1刺激引起的膜电位变化和力的产生。无钾培养基可阻止H2激活的超极化作用。就离子通量而言，发现H1激活会导致钾外流增加，而同时的H2激活只会减少H1激活引起的通量增加。H1激活诱导细胞内钙库释放钙，而H2激活则抑制这种释放。
