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异丙肾上腺素对大鼠离体心房去甲肾上腺素释放的促进作用不涉及血管紧张素II的形成。

Facilitation of noradrenaline release by isoprenaline in rat isolated atria does not involve angiotensin II formation.

作者信息

Mian M A, Majewski H, Rand M J

机构信息

Department of Pharmacology, University of Melbourne, Parkville, Victoria, Australia.

出版信息

Clin Exp Pharmacol Physiol. 1989 Dec;16(12):905-11. doi: 10.1111/j.1440-1681.1989.tb02401.x.

Abstract
  1. Rat isolated atria were incubated with 3H-noradrenaline and the intramural sympathetic nerves were stimulated at 2 Hz for 60 s. The stimulation-induced (SI) efflux of radioactivity was used as an index of release of transmitter noradrenaline. 2. Isoprenaline (0.1 mumol/L) alone did not increase noradrenaline release. Cocaine (30 mumol/L) produced a 73% increase in the stimulation-induced release of noradrenaline. In the presence of cocaine, isoprenaline enhanced noradrenaline release by 22%. 3. In the presence of cocaine, both angiotensin I (0.3 mumol/L) and angiotensin II (0.3 mumol/L) produced almost two-fold enhancements in the SI release of noradrenaline. 4. Captopril (5 mumol/L) blocked the facilitatory effect of angiotensin I on noradrenaline release but did not alter that of isoprenaline. 5. Saralasin (0.1 mumol/L) reduced the facilitatory effect of angiotensin II on noradrenaline release but did not alter that of isoprenaline. 6. The findings indicate that the facilitation of noradrenaline release by isoprenaline in rat atria is not mediated by local formation of angiotensin II.
摘要
  1. 将大鼠离体心房与3H-去甲肾上腺素一起孵育,以2 Hz的频率刺激壁内交感神经60秒。刺激诱导的放射性流出用作递质去甲肾上腺素释放的指标。2. 单独使用异丙肾上腺素(0.1 μmol/L)不会增加去甲肾上腺素的释放。可卡因(30 μmol/L)使刺激诱导的去甲肾上腺素释放增加了73%。在可卡因存在的情况下,异丙肾上腺素使去甲肾上腺素释放增加了22%。3. 在可卡因存在的情况下,血管紧张素I(0.3 μmol/L)和血管紧张素II(0.3 μmol/L)均使刺激诱导的去甲肾上腺素释放增加了近两倍。4. 卡托普利(5 μmol/L)阻断了血管紧张素I对去甲肾上腺素释放的促进作用,但未改变异丙肾上腺素的作用。5. 沙拉新(0.1 μmol/L)降低了血管紧张素II对去甲肾上腺素释放的促进作用,但未改变异丙肾上腺素的作用。6. 这些发现表明,异丙肾上腺素对大鼠心房去甲肾上腺素释放的促进作用不是由局部生成血管紧张素II介导的。

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