Satake N, Shibata S, Takagi T
Gen Pharmacol. 1986;17(5):553-8. doi: 10.1016/0306-3623(86)90092-3.
The effects of melatonin on the contractile responses to 5-hydroxytryptamine (5-HT), norepinephrine (NE), angiotensin-1 (AT-1) and potassium were determined on the rabbit isolated aorta, iliac and renal arteries. Melatonin, at 10(-4) or 10(-3) M inhibited the response to 5-HT in the aorta, iliac and renal arteries. Melatonin, at 10(-3) M, had a negligible effect on the responses to NE and AT-1 in all preparations used. The potassium-induced contraction of all 3 preparations used was slightly inhibited by only the high concentration of melatonin (10(-3) M). In a Ca+-free medium with EGTA (0.1 mM), the residual response to 5-HT (10(-5) or 10(-4) M) were inhibited by melatonin (10(-4) or 10(-3) M) in all preparations used. In a Ca2+-free medium with EGTA (0.01 mM), nifedipine (10(-6) M) and 5-HT (5 X 10(-7) M), application of Ca2+ (2 mM) resulted in a tonic contraction, related to receptor operated channels, of all preparations. This Ca2+ dependent, nifedipine insensitive contraction was markedly inhibited or abolished by melatonin at 10(-5) and 10(-4) M. These results demonstrated that melatonin had a generally greater inhibitory effect on the response to 5-HT than those to NE, AT-1 and potassium in vascular smooth muscles. Also the results suggest that action of melatonin on the 5-HT induced contraction is more related to interference with Ca2+ influx through receptor operated channels than release of intracellular Ca2+ from the store site.
在兔离体主动脉、髂动脉和肾动脉上，测定了褪黑素对5-羟色胺（5-HT）、去甲肾上腺素（NE）、血管紧张素-1（AT-1）和钾离子引起的收缩反应的影响。10⁻⁴或10⁻³M的褪黑素抑制主动脉、髂动脉和肾动脉对5-HT的反应。在所有使用的标本中，10⁻³M的褪黑素对NE和AT-1引起的反应影响可忽略不计。仅高浓度（10⁻³M）的褪黑素轻微抑制了所有3种使用标本中钾离子诱导的收缩。在含有EGTA（0.1 mM）的无钙培养基中，所有使用的标本中，褪黑素（10⁻⁴或10⁻³M）抑制了对5-HT（10⁻⁵或10⁻⁴M）的残余反应。在含有EGTA（0.01 mM）、硝苯地平（10⁻⁶M）和5-HT（5×10⁻⁷M）的无钙培养基中，施加Ca²⁺（2 mM）导致所有标本出现与受体操纵通道相关的强直收缩。这种Ca²⁺依赖性、硝苯地平不敏感的收缩在10⁻⁵和10⁻⁴M的褪黑素作用下被显著抑制或消除。这些结果表明，在血管平滑肌中，褪黑素对5-HT反应的抑制作用通常比对NE、AT-1和钾离子反应的抑制作用更强。此外，结果还表明，褪黑素对5-HT诱导收缩的作用更多地与干扰通过受体操纵通道的Ca²⁺内流有关，而不是与从储存部位释放细胞内Ca²⁺有关。
