Effect of L-NAME-induced hypertension on melatonin receptors and melatonin levels in the pineal gland and the peripheral organs of rats
Effect of L-NAME-induced hypertension on melatonin receptors and melatonin levels in the pineal gland and the peripheral organs of rats
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DOI：
10.1038/hr.2009.12
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发表时间：
2009-04-01
影响因子：
5.4
通讯作者：
Zeman, Michal
中科院分区：
文献类型：
--
作者：
Benova, Miroslava;Herichova, Iveta;Zeman, Michal
褪黑激素在血压（BP）控制中起作用。本研究的目的是确定是否褪黑激素浓度和褪黑激素受体水平的L-NAME治疗，NO缺乏性高血压大鼠的改变。两组成年雄性Wistar大鼠进行了研究：大鼠（n = 36）与NO合酶抑制剂L-NAME（40 mg kg（-1））和年龄匹配的对照组（n = 36）。每周通过尾袖体积描记法测量血压。4周后，L-NAME给药增加了BP（178 +/- 1 vs.对照组118 +/- 1 mm Hg）。给药结束时，在24小时内定期4小时处死大鼠。测定血浆、松果体、心脏和肾脏中的褪黑素浓度以及主动脉中的褪黑素受体（MT 1）密度。一个显着的褪黑激素浓度的日节律被发现在血液，松果体，肾脏和心脏的控制和高血压大鼠。L-NAME治疗组大鼠的夜间松果体褪黑素峰值浓度高于对照组（每个松果体3.38 +/- 0.48 ng vs. 1.75 +/- 0.33 ng）。两组之间没有发现血液，肾脏和心脏中的褪黑激素浓度或主动脉中的MT 1受体密度的差异。我们的研究结果表明，L-NAME治疗增强松果体中的褪黑激素的产生，可能是通过降低NO对松果体中褪黑激素产生的抑制作用。然而，增强松果体褪黑激素的形成是不足以增加褪黑激素浓度的循环，心脏和肾脏的L-NAME治疗的大鼠，表明增加使用褪黑激素在高血压动物。
Melatonin plays a role in blood pressure (BP) control. The aim of this study was to determine whether melatonin concentrations and melatonin receptor levels are altered in L-NAME-treated, NO-deficient hypertensive rats. Two groups of male adult Wistar rats were investigated: rats (n = 36) treated with NO-synthase inhibitor L-NAME (40 mg kg(-1)) and age-matched controls (n = 36). BP was measured weekly by tail-cuff plethysmography. After 4 weeks, L-NAME administration increased BP (178 +/- 1 vs. control 118 +/- 1 mm Hg). At the end of treatment, rats were killed in regular 4 h intervals over a 24-h period. Melatonin concentrations in the plasma, pineal gland, heart and kidney and melatonin receptor (MT1) density in the aorta were determined. A significant daily rhythm of melatonin concentrations was found in the blood, pineal gland, kidney and heart of both control and hypertensive rats. Peak nighttime pineal melatonin concentrations were higher in L-NAME-treated rats than in controls (3.38 +/- 0.48 vs. 1.75 +/- 0.33 ng per pineal gland). No differences between both groups were found in melatonin concentrations in blood, kidney and heart or in the MT1 receptor density in the aorta. Our results suggest that L-NAME treatment enhances melatonin production in the pineal gland, potentially by decreasing an inhibitory effect of NO on melatonin production in the pineal gland. However, the enhanced pineal melatonin formation was insufficient to increase melatonin concentrations in circulation, heart and kidney of L-NAME-treated rats, indicating an increased use of melatonin in hypertensive animals.