Okuno Tadatsune, Yabuki Akira, Shiraishi Mitsuya, Obi Takeshi, Miyamoto Atsushi
Department of Veterinary Pharmacology, Faculty of Agriculture, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan.
Comp Biochem Physiol C Toxicol Pharmacol. 2008 Apr;147(3):339-44. doi: 10.1016/j.cbpc.2007.12.002. Epub 2008 Jan 11.
We investigated the histamine responsiveness of basilar arterial rings isolated from chicken. We also examined whether endothelial cells were involved in the histamine responsiveness and in resting vascular tone. Histamine induced concentration-dependent relaxations under condition of precontraction by 5-hydroxytryptamine. The concentration-response curve for histamine was shifted to the right by diphenhydramine (a H(1) receptor antagonist), cimetidine (a H(2) receptor antagonist) and Nomega-nitro-L-arginine (L-NNA, a nitric oxide synthase inhibitor); however, indomethacin (a cyclooxygenase inhibitor) had no significant effect on it. Treatment with L-NNA shifted the concentration-response curve of histamine to the right in the presence of cimetidine, but not in the presence of diphenhydramine. Treatment with cimetidine shifted the concentration-response curve of histamine to the right in the presence of diphenhydramine. L-NNA induced a contraction but indomethacin had no effect on the resting vascular tone. These results suggest that histamine-induced relaxation is mediated via activation of H(1) receptors located on endothelial cells and H(2) receptors located on smooth muscle cells. The main relaxing factor released from endothelial cells is probably nitric oxide. The resting vascular tone was modulated by spontaneously released nitric oxide, but not by prostaglandins or thromboxane A(2).
我们研究了从鸡分离出的基底动脉环对组胺的反应性。我们还检查了内皮细胞是否参与组胺反应性和静息血管张力。在5-羟色胺预收缩的条件下，组胺诱导浓度依赖性舒张。组胺的浓度-反应曲线被苯海拉明（一种H(1)受体拮抗剂）、西咪替丁（一种H(2)受体拮抗剂）和Nω-硝基-L-精氨酸（L-NNA，一种一氧化氮合酶抑制剂）向右移动；然而，吲哚美辛（一种环氧化酶抑制剂）对其没有显著影响。在西咪替丁存在的情况下，L-NNA使组胺的浓度-反应曲线向右移动，但在苯海拉明存在的情况下则不然。在苯海拉明存在的情况下，西咪替丁使组胺的浓度-反应曲线向右移动。L-NNA诱导收缩，但吲哚美辛对静息血管张力没有影响。这些结果表明，组胺诱导的舒张是通过激活内皮细胞上的H(1)受体和平滑肌细胞上的H(2)受体介导的。内皮细胞释放的主要舒张因子可能是一氧化氮。静息血管张力受自发释放的一氧化氮调节，但不受前列腺素或血栓素A(2)调节。
