Impaired basal sympathetic tone and alpha1-adrenergic responsiveness in association with the hypotensive effect of melatonin in spontaneously hypertensive rats.
Impaired basal sympathetic tone and alpha1-adrenergic responsiveness in association with the hypotensive effect of melatonin in spontaneously hypertensive rats.
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发表时间：
1998
影响因子：
3.2
通讯作者：
A. K-Laflamme;L. Wu;S. Foucart;J. de Champlain
中科院分区：
文献类型：
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作者：
A. K-Laflamme;L. Wu;S. Foucart;J. de Champlain
早期的研究表明高血压与褪黑激素（一种松果体激素）之间存在关系。本研究的目的是评估交感神经系统在褪黑素对有意识的12周龄自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）的急性血压影响中的作用，并确定褪黑素的降压作用是否与突触前或突触后机制的改变有关。褪黑素（10 mg/kg）仅在SHR中产生持续的时间依赖性平均动脉压降低，而两组的心率均未发生变化。直到褪黑素给药后20分钟，两组血浆肾上腺素（EPI）水平均下降约60%，但去甲肾上腺素（NE）水平仅在SHR组下降约30%。两组在服用褪黑激素之前或之后，硝普西诱导的低血压反应和相关的心率增加相似。出乎意料的是，在褪黑激素治疗后，WKY和SHR患者对硝普苷的交感反应性（通过NE和EPI的增加来评估）均显著增强。褪黑素未改变SHR患者离体心房释放[3H]-去甲肾上腺素的刺激。在培养的主动脉血管平滑肌细胞中，基底和苯肾上腺素诱导的肌醇磷酸形成在SHR中更大，褪黑素预处理剂量依赖性地减弱了WKY和SHR细胞中苯肾上腺素的反应。因此，褪黑素的降压作用似乎与抑制基底交感肾上腺张力有关，也可能部分通过阻断突触后α - 1肾上腺素能受体诱导的肌醇磷酸形成来介导。
Early investigations have suggested a relationship between hypertension and melatonin, a pineal hormone. The aims of this study were to evaluate the implication of the sympathetic nervous system in the acute effect of melatonin on blood pressure in conscious 12-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), and to determine whether the hypotensive effect of melatonin is associated with alterations in pre- or postsynaptic mechanisms. Melatonin, 10 mg/kg, produced a sustained time-dependent decrease of mean arterial pressure only in SHR without changes in heart rate in both groups. Until 20 min after melatonin administration, plasma epinephrine (EPI) levels were reduced by about 60% in both groups, but norepinephrine (NE) levels were decreased only in SHR by about 30%. The nitroprusside-induced hypotension responses and the associated increases in heart rate were similar in both groups before or after administration of melatonin. Unexpectedly, the sympathetic reactivity to nitroprusside, evaluated by the increases in NE and EPI, was markedly enhanced after melatonin treatment in both WKY and SHR. The stimulation induced [3H]-norepinephrine release from isolated atria was not altered by melatonin in SHR. In cultured aortic vascular smooth muscle cells, the basal and phenylephrine induced inositol phosphate formations were greater in SHR, and the melatonin pretreatment dose dependently attenuated the phenylephrine responses in cells from both WKY and SHR. Therefore the hypotensive action of melatonin appears to be associated with an inhibition of basal sympathoadrenal tone and could also be mediated partly by the blockade of postsynaptic alpha1-adrenergic receptor-induced inositol phosphate formation.