Kawasaki H, Nuki C, Saito A, Takasaki K
Department of Pharmacology, Miyazaki Medical College, Japan.
Am J Physiol. 1991 Sep;261(3 Pt 2):H683-90. doi: 10.1152/ajpheart.1991.261.3.H683.
The effect of neuropeptide Y (NPY) in neurotransmission of calcitonin gene-related peptide (CGRP)-containing vasodilator nerves was investigated in rats. In perfused mesenteric vascular beds with active tone, perivascular nerve stimulation (PNS; 1-8 Hz) caused a frequency-dependent vasodilator response, which was abolished by 300 nM tetrodotoxin (TTX), 500 nM capsaicin, 1 microM human CGRP-(8-37), or cold storage denervation (4 degrees C for 72 h). NPY (5, 10, and 50 nM) concentration dependently inhibited the vasodilator response to PNS, whereas NPY had little effect on vasodilation induced by exogenous CGRP (10 and 100 pmol) or 1 nmol acetylcholine (ACh). NPY (10 nM) inhibited the neurogenic release of CGRP-like immunoreactivity induced by PNS (4 and 8 Hz), which was abolished by 300 nM TTX and the removal of Ca2+ from the medium. Combined perfusion with 5 nM NPY and 10 nM norepinephrine additively inhibited the vasodilator response to PNS but not to exogenous CGRP and ACh. Immunohistochemistry showed the distinct distribution of CGRP- and NPY-like immunoreactivity-containing fibers in rat mesenteric arteries. These results suggest that NPY modulates presynaptically the release of CGRP from CGRP-containing vasodilator nerves in rat mesenteric arteries.
在大鼠中研究了神经肽Y（NPY）对含降钙素基因相关肽（CGRP）的血管舒张神经神经传递的影响。在具有主动张力的灌注肠系膜血管床中，血管周围神经刺激（PNS；1 - 8Hz）引起频率依赖性血管舒张反应，该反应被300nM河豚毒素（TTX）、500nM辣椒素、1μM人CGRP -（8 - 37）或冷藏去神经（4℃72小时）消除。NPY（5、10和50nM）浓度依赖性地抑制对PNS的血管舒张反应，而NPY对外源性CGRP（10和100pmol）或1nmol乙酰胆碱（ACh）诱导的血管舒张几乎没有影响。NPY（10nM）抑制PNS（4和8Hz）诱导的CGRP样免疫反应性的神经源性释放，该反应被300nM TTX和从培养基中去除Ca2 +消除。5nM NPY和10nM去甲肾上腺素联合灌注可相加性抑制对PNS的血管舒张反应，但不抑制对外源性CGRP和ACh的反应。免疫组织化学显示大鼠肠系膜动脉中含CGRP和NPY样免疫反应性纤维的不同分布。这些结果表明，NPY在突触前调节大鼠肠系膜动脉中含CGRP的血管舒张神经释放CGRP。
