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NG-单甲基-L-精氨酸对大鼠肠系膜阻力动脉β-肾上腺素能受体介导的舒张作用。

Effect of NG-monomethyl-L-arginine on the beta-adrenoceptor-mediated relaxation of rat mesenteric resistance arteries.

作者信息

Blankesteijn W M, Thien T

机构信息

Dept. of Medicine, University Hospital Nijmegen, The Netherlands.

出版信息

Life Sci. 1993;52(16):PL135-9. doi: 10.1016/0024-3205(93)90178-6.

Abstract

beta-Adrenoceptors are present on vascular smooth muscle and on endothelium. We investigated whether the endothelial beta-adrenoceptors induce relaxation of rat mesenteric resistance arteries by stimulation of endothelium-derived relaxing factor (EDRF) release. To this end, the relaxation was studied in the presence and absence of 100 microM NG-monomethyl-L-arginine (L-NMMA), a specific inhibitor of the production of EDRF. The maximal relaxation with isoprenaline, expressed as a percentage of the precontraction, was 44.0 +/- 4.0% (n = 12) in the L-NMMA treated group and 58.0 +/- 2.6% (n = 13) in the untreated group, a statistically significant difference (P = 0.008). However, the precontraction with 40 mM K+ tended to be higher in the presence of L-NMMA. The pD2-value for isoprenaline was not significantly changed by the L-NMMA treatment. We conclude that the isoprenaline-mediated relaxation of mesenteric resistance arteries is inhibited by L-NMMA, but that this effect can at least in part be ascribed to an inhibition of baseline EDRF-release.

摘要

β-肾上腺素能受体存在于血管平滑肌和内皮细胞上。我们研究了内皮β-肾上腺素能受体是否通过刺激内皮衍生舒张因子(EDRF)释放来诱导大鼠肠系膜阻力动脉舒张。为此,在存在和不存在100微摩尔NG-单甲基-L-精氨酸(L-NMMA,一种EDRF产生的特异性抑制剂)的情况下研究舒张情况。用异丙肾上腺素诱导的最大舒张,以预收缩的百分比表示,在L-NMMA处理组中为44.0±4.0%(n = 12),在未处理组中为58.0±2.6%(n = 13),差异有统计学意义(P = 0.008)。然而,在L-NMMA存在的情况下,用40毫摩尔钾诱导的预收缩往往更高。L-NMMA处理对异丙肾上腺素的pD2值没有显著影响。我们得出结论,L-NMMA抑制了异丙肾上腺素介导的肠系膜阻力动脉舒张,但这种作用至少部分可归因于对基础EDRF释放的抑制。

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