ENDOTHELIUM-DERIVED NITRIC-OXIDE AND CYCLOOXYGENASE PRODUCTS MODULATE CORPUS CAVERNOSUM SMOOTH-MUSCLE TONE
ENDOTHELIUM-DERIVED NITRIC-OXIDE AND CYCLOOXYGENASE PRODUCTS MODULATE CORPUS CAVERNOSUM SMOOTH-MUSCLE TONE
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DOI：
10.1016/s0022-5347(17)37201-4
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发表时间：
1992-01-01
影响因子：
6.6
通讯作者：
DETEJADA, IS
中科院分区：
文献类型：
--
作者：
AZADZOI, KM;KIM, N;DETEJADA, IS
阴茎海绵体平滑肌的舒张受神经和内皮源性物质的控制。 在这项研究中，海绵体平滑肌的内皮依赖性舒张的特点和花生四烯酸产品的环氧合酶在内皮依赖性舒张的作用进行了检查。 通过输注3-[（3-胆酰胺丙基）-二甲基铵基]-1-丙磺酸盐从兔体中去除内皮细胞，并通过透射电子显微镜证实。 在器官室中对人和兔的身体组织条进行等长张力测量。 通过放射免疫测定法测定了环磷酸鸟苷（cGMP）的积累和从身体组织释放的类花生酸，并与平滑肌松弛相关。 我们的研究表明，海绵体组织对乙酰胆碱，缓激肽和P物质的舒张是内皮依赖性的;吲哚美辛增强; N（G）-单甲基-L-精氨酸，亚甲蓝或LY 83583抑制。 罂粟碱和硝普钠的舒张作用不依赖于内皮，不受N（G）-单甲基-L-精氨酸的影响。 血管活性肠肽的舒张作用部分依赖于内皮细胞;吲哚美辛可增强舒张作用; N（G）-单甲基-L-精氨酸或亚甲蓝可减弱舒张作用。 乙酰胆碱和一氧化氮可使组织cGMP水平升高。 亚甲蓝抑制cGMP的基础和药物刺激水平。 乙酰胆碱可促进类花生酸的释放，吲哚美辛可阻断类花生酸的释放。 总之，一氧化氮或一种密切相关的物质占的活性内皮衍生的舒张因子在身体组织。 抑制类花生酸的释放增强了一氧化氮的舒张作用。 一氧化氮增加组织cGMP，其似乎调节身体平滑肌松弛。
Relaxation of penile corpus cavernosum smooth muscle is controlled by nerve and endothelium derived substances. In this study, endothelium-dependent relaxation of corporal smooth muscle was characterized and the role of arachidonic acid products of cyclooxygenase in endothelium-dependent relaxation was examined. Endothelium removal from rabbit corpora was performed by infusion with 3-[(3-cholamidopropyl)-dimethylammonio]-1-propane sulfonate and was confirmed by transmission electron microscopy. Strips of human and rabbit corporal tissues were studied in the organ chambers for isometric tension measurement. The accumulation of cyclic guanosine monophosphate (cGMP) and the release of eicosanoids from corporal tissue was measured by radioimmunoassay and correlated to smooth muscle relaxation. Our study showed that relaxation of corpus cavernosum tissue to acetylcholine, bradykinin and substance P was endothelium-dependent; potentiated by indomethacin; and inhibited by N(G)-monomethyl-L-arginine, methylene blue or LY83583. Relaxation to papaverine and sodium nitroprusside was endothelium-independent, and unaffected by N(G)-monomethyl-L-arginine. Relaxation to vasoactive intestinal polypeptide was partially endothelium-dependent; potentiated by indomethacin; attenuated by N(G)-monomethyl-L-arginine or methylene blue. The tissue level of cGMP was enhanced by acetylcholine and nitric oxide. Methylene blue inhibited both basal and drug-stimulated levels of cGMP. The release of eicosanoids was enhanced by acetylcholine and blocked by indomethacin. In conclusion, nitric oxide or a closely related substance accounts for the activity of endothelium-derived relaxing factor in the corporal tissue. Inhibition of the release of eicosanoids potentiates the relaxing effect of nitric oxide. Nitric oxide increases tissue cGMP which appears to modulate corporal smooth muscle relaxation.