Edvinsson L
Acta Physiol Scand. 1985 Sep;125(1):33-41. doi: 10.1111/j.1748-1716.1985.tb07690.x.
The action of neuropeptide Y (NPY), which coexists with noradrenaline (NA) in perivascular sympathetic nerves, has been examined on feline cerebrovascular smooth muscle using a sensitive in vitro system. The direct cerebrovascular responses of peptides with structural similarities with NPY, peptide YY (PYY), avian (APP), and bovine (BPP) and human (HPP) pancreatic polypeptides, have been compared with that of NPY on isolated feline cerebral arteries. The relative potency for contractions induced by the peptides is: NPY, PYY greater than APP greater than BPP, HPP. The alpha-adrenoceptor antagonist rauwolscine, which blocked the response to noradrenaline (NA), had no effect on NPY-induced contractions. Neuropeptide Y significantly potentiated contractions induced by 10(-6) M NA, but not by 10(-5) M. Withdrawal of Ca2+ from the extracellular medium for 30 min reduced the contractile response to NPY in cerebral vessels by about 80%. Subsequent readdition of Ca2+ caused reproducible contractions which were inhibited by the calcium entry blocker nimodipine. Nimodipine also relaxed isolated middle cerebral artery segments contracted by NPY and NA in a concentration-dependent manner. The data suggest that NPY mediates contraction of cerebrovascular smooth muscle via a mechanism that is dependent on the concentration of extracellular calcium.
在一种灵敏的体外系统中,研究了与去甲肾上腺素(NA)共存于血管周围交感神经中的神经肽Y(NPY)对猫脑血管平滑肌的作用。在分离的猫脑动脉上,将与NPY结构相似的肽,即肽YY(PYY)、禽胰多肽(APP)、牛胰多肽(BPP)和人胰多肽(HPP)的直接脑血管反应与NPY的反应进行了比较。这些肽诱导收缩的相对效力为:NPY、PYY大于APP大于BPP、HPP。阻断对去甲肾上腺素(NA)反应的α-肾上腺素能受体拮抗剂育亨宾,对NPY诱导的收缩没有影响。神经肽Y显著增强了10⁻⁶ M NA诱导的收缩,但对10⁻⁵ M NA诱导的收缩没有增强作用。从细胞外培养基中去除Ca²⁺ 30分钟,可使脑血管对NPY的收缩反应降低约80%。随后重新添加Ca²⁺ 会引起可重复的收缩,而这种收缩会被钙通道阻滞剂尼莫地平抑制。尼莫地平还以浓度依赖的方式舒张由NPY和NA收缩的分离大脑中动脉节段。数据表明,NPY通过一种依赖于细胞外钙浓度的机制介导脑血管平滑肌的收缩。