Mechanisms of postjunctional synergism between adenosine 5'-triphosphate (ATP) and noradrenaline were studied in isolated guinea pig vas deferens. Whereas prior exposure to ATP had no significant effect on noradrenaline-mediated contractions, noradrenaline concentration-dependently enhanced ATP-induced contractions. Similarly to noradrenaline, histamine, which also acts via phospholipase-coupled receptors, induced contractions of the vas deferens and enhanced subsequent responses to ATP. Although phorbol-12, 13-dibutyrate (PDBu), a stimulant of protein kinase C (PKC), failed to induce contractions, it significantly potentiated ATP-induced contractions. The PKC inhibitor, Calphostin C, prevented this effect and the noradrenaline-mediated enhancement of ATP-induced contractions. The phosphatase inhibitor cantharidin induced a time- and concentration-dependent tonic contraction and markedly increased subsequent contractions to ATP. It is suggested that noradrenaline potentiates the contractile response of the vas deferens to ATP via a PKC-mediated mechanism. This may involve the inhibition of myosin light chain phosphatase (MLCP) and subsequent calcium sensitisation.

译文

在分离的豚鼠输精管中研究了5 '-三磷酸腺苷 (ATP) 和去甲肾上腺素之间的结后协同作用机制。尽管先前暴露于ATP对去甲肾上腺素介导的收缩没有显着影响,但去甲肾上腺素浓度依赖性地增强了ATP诱导的收缩。与去甲肾上腺素类似,组胺也通过磷脂酶偶联受体起作用,可诱导输精管收缩并增强对ATP的后续反应。尽管phorbol-12,13-二丁酸 (PDBu),一种蛋白激酶C (PKC) 的刺激物,未能诱导收缩,但它显著增强了ATP诱导的收缩。PKC抑制剂Calphostin C阻止了这种作用以及去甲肾上腺素介导的ATP诱导的收缩的增强。磷酸酶抑制剂斑霉素可诱导时间和浓度依赖性的强直收缩,并显着增加随后对ATP的收缩。建议去甲肾上腺素通过PKC介导的机制增强输精管对ATP的收缩反应。这可能涉及抑制肌球蛋白轻链磷酸酶 (MLCP) 和随后的钙致敏。

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