Ueno Y, Arita M, Suruda H, Ohtani H, Minakata T, Kuchii M, Nishio I, Masuyama Y
Jpn Circ J. 1980 Dec;44(12):981-7. doi: 10.1253/jcj.44.981.
In order to evaluate the role of the renin-angiotensin system and the sympathetic nervous system in the maintenance of blood pressure in the sodium-depleted state, the changes of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and plasma noradrenaline (PNA) were examined in unanesthetized dogs after the administration of furosemide. Furthermore, the role of the renin-angiotensin system in the increased sympathetic nerve activity induced by furosemide was assessed by using Sar1-Ile8-angiotensin II, an angiotensin II antagonist. When a dose of 0.8 mg/kg of furosemide was injected intravenously, 3 times every 15 minutes, PRA and PNA were significantly increased with a concomitant increase in PAC. Sar1-Ile8-angiotensin II induced a significant increase in PAC and a slight increase in PRA, while no changes were found in PNA and the mean blood pressure. The increase in PNA induced by furosemide was inhibited dose-dependently by Sar1-Ile8-angiotensin II, through PRA and PAC were further increased. There results suggest that an administration of furosemide induced the increase in PNA and the increase in PNA by furosemide might by mediated by the renin-angiotensin system.
为了评估肾素 - 血管紧张素系统和交感神经系统在维持缺钠状态下血压中的作用，在未麻醉的犬静脉注射速尿后，检测血浆肾素活性（PRA）、血浆醛固酮浓度（PAC）和血浆去甲肾上腺素（PNA）的变化。此外，通过使用血管紧张素II拮抗剂Sar1 - Ile8 - 血管紧张素II评估肾素 - 血管紧张素系统在速尿诱导的交感神经活性增加中的作用。当以0.8mg/kg的剂量静脉注射速尿，每15分钟注射3次时，PRA和PNA显著增加，同时PAC也增加。Sar1 - Ile8 - 血管紧张素II使PAC显著增加，PRA略有增加，而PNA和平均血压无变化。Sar1 - Ile8 - 血管紧张素II剂量依赖性地抑制了速尿诱导的PNA增加，尽管PRA和PAC进一步增加。这些结果表明，速尿给药诱导了PNA增加，且速尿诱导的PNA增加可能由肾素 - 血管紧张素系统介导。
