Donald John A, Broughton Brad R S, Bennett Michael B
School of Biological and Chemical Sciences, Deakin University, Pigdons Road, Geelong, VIC 3217, Australia.
Comp Biochem Physiol A Mol Integr Physiol. 2004 Jan;137(1):21-31. doi: 10.1016/s1095-6433(03)00260-5.
This study investigated the nature of vasodilator mechanisms in the dorsal aorta of the giant shovelnose ray, Rhinobatus typus. Anatomical techniques found no evidence for an endothelial nitric oxide synthase, but neural nitric oxide synthase was found to be present in the perivascular nerve fibres of the dorsal aorta and other arteries and veins using both NADPH-diaphorase staining and immunohistochemistry with a specific neural NOS antibody. Arteries and veins both contained large nNOS-positive nerve trunks from which smaller nNOS-positive bundles branched and formed a plexus in the vessel wall. Single, varicose nNOS-positive nerve fibres were present in both arteries and veins. Within the large bundles of both arteries and veins, groups of nNOS-positive cell bodies forming microganglia were observed. Double-labelling immunohistochemistry using an antibody to tyrosine hydroxylase showed that nearly all the NOS nerves were not sympathetic. Acetylcholine always caused constriction of isolated rings of the dorsal aorta and the nitric oxide donor, sodium nitroprusside, did not mediate any dilation. Addition of nicotine (3 x 10(-4) M) to preconstricted rings caused a vasodilation that was not affected by the nitric oxide synthase inhibitor, L-NNA (10(-4) M), nor the soluble guanylyl cyclase inhibitor, ODQ (10(-5) M). This nicotine-mediated vasodilation was, therefore, not due to the synthesis and release of NO. Disruption of the endothelium significantly reduced or eliminated the nicotine-mediated vasodilation. In addition, indomethacin (10(-5) M), an inhibitor of cyclooxygenases, significantly increased the time period to maximal dilation and reduced, but did not completely inhibit the nicotine-mediated vasodilation. These data support the hypothesis that a prostaglandin is released from the vascular endothelium of a batoid ray, as has been described previously in other groups of fishes. The function of the nitrergic innervation of the blood vessels is not known because nitric oxide does not appear to regulate vascular tone.
本研究调查了巨型铲鼻鳐（Rhinobatus typus）背主动脉中血管舒张机制的本质。解剖技术未发现内皮型一氧化氮合酶的证据，但使用NADPH-黄递酶染色和特异性神经型一氧化氮合酶抗体进行免疫组织化学检测发现，背主动脉及其他动脉和静脉的血管周围神经纤维中存在神经型一氧化氮合酶。动脉和静脉均含有大型nNOS阳性神经干，较小的nNOS阳性束从这些神经干分支出来，并在血管壁形成神经丛。动脉和静脉中均存在单个、曲张的nNOS阳性神经纤维。在动脉和静脉的大型束内，观察到形成微神经节的nNOS阳性细胞体群。使用酪氨酸羟化酶抗体进行双标免疫组织化学显示，几乎所有的NOS神经都不是交感神经。乙酰胆碱总是引起背主动脉分离环的收缩，一氧化氮供体硝普钠不介导任何舒张。向预收缩环中加入尼古丁（3×10⁻⁴ M）会引起血管舒张，该舒张不受一氧化氮合酶抑制剂L-NNA（10⁻⁴ M）和可溶性鸟苷酸环化酶抑制剂ODQ（10⁻⁵ M）的影响。因此，这种尼古丁介导的血管舒张不是由于NO的合成和释放。内皮破坏显著降低或消除了尼古丁介导的血管舒张。此外，环氧化酶抑制剂吲哚美辛（10⁻⁵ M）显著延长了达到最大舒张的时间，并降低了但未完全抑制尼古丁介导的血管舒张。这些数据支持了这样一种假说，即如先前在其他鱼类群体中所描述的那样，一种前列腺素从鳐类的血管内皮释放。血管的氮能神经支配功能尚不清楚，因为一氧化氮似乎不调节血管张力。
