Zawilska J B, Nowak J Z
Department of Pharmacodynamics, Polish Academy of Sciences, Lodz.
J Neural Transm Gen Sect. 1991;84(3):171-82. doi: 10.1007/BF01244968.
The effects of different organic compounds that block and increase Ca2+ influx through the voltage-sensitive calcium channels (VSCC) on the nocturnal serotonin N-acetyltransferase (NAT) activity was investigated in vivo in rats. Systemic administration of VSCC antagonists, i.e. nimodipine, nifedipine, verapamil and diltiazem, resulted in a marked suppression of the nighttime pineal NAT activity. Bay K 8644, a VSCC agonist, injected to rats before the time of the light offset of the light-dark cycle significantly enhanced the nocturnal increase of the pineal NAT activity. Although Bay K 8644 given during the dark phase of an imposed illumination cycle had little effect on the nocturnal pineal NAT activity, it antagonized the nimodipine- and verapamil-induced decrease in the enzyme activity. These results support the role of Ca2+ influx through the VSCC in the nocturnal increase of NAT activity in the pineal gland of rat.
在大鼠体内研究了不同有机化合物通过电压敏感性钙通道(VSCC)阻断和增加Ca2+内流对夜间血清素N-乙酰基转移酶(NAT)活性的影响。全身给予VSCC拮抗剂,即尼莫地平、硝苯地平、维拉帕米和地尔硫䓬,导致夜间松果体NAT活性显著抑制。在明暗周期的光照偏移时间之前给大鼠注射VSCC激动剂Bay K 8644,可显著增强松果体NAT活性的夜间增加。尽管在强制光照周期的黑暗阶段给予Bay K 8644对夜间松果体NAT活性几乎没有影响,但它拮抗了尼莫地平和维拉帕米诱导的酶活性降低。这些结果支持了通过VSCC的Ca2+内流在大鼠松果体NAT活性夜间增加中的作用。