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Abstract:
The purpose of this study was to determine the effects of 17β-estradiol
(E2) on electrical activity of the rostral ventrolateral medulla (RVLM)
neurons in rats. Male Sprague-Dawley rats were anesthetized with urethane
(1.0 g/kg) and subjected to sino-aortic denervation. Blood pressure, heart
rate and spontaneous discharge of RVLM neurons were recorded
simultaneously. Intracarotid injection of E2 (10 ng/kg) decreased the
discharge rate from 14.46±0.47
to 9.73±0.33
spikes/s (P<0.001) in 25 out of 30 RVLM neurons, while blood pressure and
heart rate showed no significant change. The inhibitory effect of E2 on
RVLM neuronal activity was rapid at the onset (within 1 min) and
long-lasting (>5 min). Prior administration of antiestrogen tamoxifen
(TAM) did not affect the effect of E2. However, pretreatment with Nω-nitro-L-arginine-methyl
ester (L-NAME), an inhibitor of nitric oxide (NO) synthase, significantly
atte
nuated the inhibitory effect of E2. In addition, NO donor
3-morpholinosydnonimine (SIN-1) potentiated the effect of E2. These
results suggest that E2 may inhibit spontaneous electrical activity of
RVLM neurons, an effect which is mediated by the activation of NOS with
the resultant of NO release via nongenomic actions.
Key words:
estrogen; rostral ventrolateral medulla; spontaneous discharge; nitric
oxide
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王升,
何瑞荣*
(河北医科大学基础医学研究所生理室,
石家庄
050017)
摘 要:
本研究旨在观察17β-雌二醇(E2)对雄性大鼠延髓腹外侧头端区(RVLM)神经元自发放电活动的影响。在切断双侧缓冲神经的麻醉雄性Sprague-Dawley大鼠上,
同步记录血压、
心率和RVLM神经元的自发放电活动。颈动脉内注射E2
(10 ng/kg), 30个RVLM神经元自发放电单位中有25个单位的放电频率由14.46±0.47降至9.73±0.33
spikes/s (P<0.05),
与此同时血压和心率无明显改变。E2的抑制效应在1
min内起效,
持续时间长于5
min。
雌激素受体拮抗剂tamoxifen
(5 mg/kg)不能阻断E2
的抑制效应。预先给予一氧化氮(NO)合酶阻断剂L-NAME
(2.7 μg/kg)能明显阻断E2的抑制效应。应用NO供体SIN-1
(0.5 μg/kg)可增强E2的抑制效应。以上结果提示,
E2可通过非基因组效应激活RVLM神经元的NOS而引发NO释放,
进而抑制其自发放电活动。
关键词:
雌激素;
延髓腹外侧头端区;
自发放电;
一氧化氮
学科分类号:
Q463; R331.3 |
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