Maggi C A, Patacchini R, Santicioli P, Giuliani S, Geppetti P, Meli A
Pharmacology Department, Research Laboratories, A. Menarini Pharmaceuticals, Florence, Italy.
Neurosci Lett. 1988 May 26;88(2):201-5. doi: 10.1016/0304-3940(88)90126-7.
In the rat isolated urinary bladder, exposure to capsaicin (1 microM) produced a contraction thought to involve neuropeptide(s) release from sensory nerves. A second application of the drug had no motor effect indicating desensitization. The establishment of the desensitized state requires the presence of extracellular calcium. In the presence of Ruthenium red 9RR, 30 nM-10 microM) the first response to capsaicin was reduced and a concentration-dependent protection from capsaicin desensitization was observed. RR up to 10 microM had no inhibitory effect toward contractions produced by exogenous substance P nor by electrical stimulation of efferent nerves.
在大鼠离体膀胱中，暴露于辣椒素（1微摩尔）会引起收缩，这种收缩被认为涉及感觉神经释放神经肽。再次应用该药物没有运动效应，表明出现了脱敏现象。脱敏状态的建立需要细胞外钙的存在。在钌红（9RR，30纳摩尔 - 10微摩尔）存在的情况下，对辣椒素的首次反应减弱，并且观察到对辣椒素脱敏具有浓度依赖性保护作用。高达10微摩尔的RR对外源性P物质引起的收缩或传出神经的电刺激引起的收缩均无抑制作用。
