Sodium nitroprusside and other smooth muscle-relaxants increase cyclic GMP levels in rat ductus deferens

Sodium nitroprusside and other smooth muscle-relaxants increase cyclic GMP levels in rat ductus deferens
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硝普钠和其他平滑肌松弛剂增加大鼠输精管中的环 GMP 水平

DOI:
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发表时间:
1977
期刊:
影响因子:
64.8
通讯作者:
G. Schultz
G. Schultz
中科院分区:
综合性期刊1区
文献类型:
--
作者:
K. Schultz;K. Schultz;G. Schultz

文献摘要

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平滑肌张力似乎主要受细胞质中游离钙浓度的调节1,2。引起平滑肌收缩的几种药物增加了组织中环GMP的含量,而环AMP浓度没有显著变化或仅略有降低3 -7。已经证实5 -7,环鸟苷酸可能偶然参与平滑肌的收缩反应,并且这种核苷酸可能与钙一起作为喜剧演员来促进收缩。然而,一些观察结果与这一假设并不一致。虽然激素和神经递质诱导的组织张力增加1,2和环GMP水平增加8 -10通常依赖于细胞外钙的存在,并且似乎是继发于钙流入细胞质的增加,但这两种钙依赖性事件之间的相关性在各种组织中很差10 -16。基于这些观察结果,我们认为环鸟苷酸可能作为一种负反馈抑制剂,抑制经尿道刺激的钙离子流入细胞质8,10,11。我们研究了各种药物对大鼠输精管中环核苷酸水平的影响,并在这里报告,许多平滑肌松弛剂,包括硝普钠(SNP),增加环GMP水平在输精管。
SMOOTH muscle tone seems to be primarily regulated by the concentration of free calcium in cytoplasm1,2. Several agents that cause smooth muscle contraction increase the tissue content of cyclic GMP with no significant change or only small reduction of the cyclic AMP concentration3–7. It has been suggested5–7 that cyclic GMP may be casually involved in the contractile response of smooth muscle and that this nucleotide may act as a comediator with calcium to promote contraction. Several observations, however, are not consistent with this assumption. Although increases both in tissue tonus1,2 and in the cyclic GMP level8–10 induced by hormones and neurotransmitters are generally dependent on the presence of extracellular calcium and seem to be secondary to increased influx of calcium into the cytoplasm, the correlation between these two calcium-dependent events is poor in various tissues10–16. On the basis of such observations, we have suggested that cyclic GMP may act as a negative feedback inhibitor of hormonally stimulated calcium influx into cytoplasm8,10,11. We have studied the effects of various agents on cyclic nucleotide levels in the ductus deferens of the rat, and report here that many smooth muscle relaxants, including sodium nitroprusside (SNP), increase cyclic GMP levels in the ductus deferens.