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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Characterization of the vasorelaxation to methanandamide in rat gastric arteries.
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Characterization of the vasorelaxation to methanandamide in rat gastric arteries.

机译：在大鼠胃动脉血管舒张为甲烷和酰胺的特征。

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摘要

In the present study, the relaxant effect of the cannabinoid methanandamide was explored in rat gastric arteries. Since in some vessels cannabinoids have been shown to release calcitonin gene-related peptide (CGRP) from perivascular nerves, the influence of methanandamide was compared with that of exogenous CGRP. Methanandamide and CGRP elicited concentration-dependent, endothelium-independent relaxations. Methanandamide-induced relaxations were unaffected by the CB1 receptor antagonist AM251, the CB2 receptor antagonists AM630 and SR144528, and combined pre-exposure to AM251 and SR144528. Pre-exposure to O-1918, an antagonist of a novel nonCB1onCB2 cannabinoid receptor, did not influence the relaxations to methanandamide. Capsaicin or capsazepine treatment slightly inhibited methanandamide-induced relaxations. Preincubation with 30 mmol/L extracellular K+ or 3 mmol/L TEA had no significant effect on the responses elicited by methanandamide, but reduced CGRP-induced relaxations. Relaxation to 10-5 mol/L methanandamide was significantly blunted by Bay K8644 and by preincubation with nifedipine. Furthermore, 10-5 mol/L methanandamide significantly inhibited CaCl2-induced contractions in norepinephrine-stimulated vessels previously depleted of intra- and extracellular Ca2+. Finally, preincubation with 10-5 mol/L methanandamide almost completely abolished high K+-induced contractions. These findings suggest that the vasorelaxant action of methanandamide in rat gastric arteries is not mediated by stimulation of known cannabinoid receptors and only partly related to stimulation of TRPV1 receptors on perivascular nerves. At high concentrations, methanandamide might induce relaxation by reducing calcium entry into the smooth muscle cells.
机译：在本研究中，研究了大麻素甲than胺在大鼠胃动脉中的放松作用。由于大麻素已显示在某些血管中可从血管周围神经释放降钙素基因相关肽（CGRP），因此将甲烷和酰胺的影响与外源性CGRP进行了比较。甲烷甲酰胺和CGRP引起浓度依赖性，内皮依赖性松弛。甲乙酰胺诱导的弛豫不受CB1受体拮抗剂AM251，CB2受体拮抗剂AM630和SR144528的影响，并与AM251和SR144528的预暴露相结合。预先暴露于新型非CB1 / nonCB2大麻素受体的拮抗剂O-1918不会影响到甲than酰胺的松弛。辣椒素或辣椒素治疗可轻微抑制甲烷和酰胺诱导的松弛。用30 mmol / L胞外K +或3 mmol / L TEA进行预培养对甲than酰胺引起的反应无明显影响，但减少了CGRP引起的松弛。 Bay K8644以及与硝苯地平一起预温育可明显减弱松弛至10-5 mol / L的甲酰胺。此外，10-5 mol / L甲氨酰胺可显着抑制去甲肾上腺素刺激的血管内先前由细胞内和细胞外Ca2 +耗竭的CaCl2诱导的收缩。最终，与10-5 mol / L甲烷甲酰胺的预孵育几乎完全消除了高K +诱导的收缩。这些发现表明，甲乙酰胺在大鼠胃动脉中的血管舒张作用不是由已知大麻素受体的刺激介导的，而仅部分与血管周神经上TRPV1受体的刺激有关。在高浓度下，甲烷甲酰胺可能会通过减少钙进入平滑肌细胞来诱导松弛。

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