Carrière S, Cardinal J, LeGrimellec C
Can J Physiol Pharmacol. 1979 Jul;57(7):681-7. doi: 10.1139/y79-103.
Norepinephrine (NE) release and pressor response to sympathetic stimulation were studied in dogs under furosemide-induced acute volume depletion. The rise in blood pressure observed following carotid clamping proved similar before and after acute salt and water depletion in the first group of animals and NE rose comparably in these two conditions. Similar results were obtained in a second group of dogs that received an angiotensin II converting enzyme inhibitor (CEI). This study shows that contrary to isotonic saline loading, acute salt and water depletion cause a progressive increase in NE plasma levels. Moreover, these results clearly demonstrate that the decrease in sympatho--adrenergic response and the predominant role played by the renin--aniotensin system during chronic salt depletion are not observed in acute conditions.
在速尿诱导的急性容量耗竭状态下，对犬去甲肾上腺素（NE）释放及交感神经刺激的升压反应进行了研究。在第一组动物中，急性盐和水耗竭前后，颈动脉夹闭后观察到的血压升高情况相似，且在这两种情况下NE升高程度相当。在接受血管紧张素II转换酶抑制剂（CEI）的第二组犬中也得到了类似结果。本研究表明，与等渗盐水负荷情况相反，急性盐和水耗竭会导致血浆NE水平逐渐升高。此外，这些结果清楚地表明，在急性情况下未观察到慢性盐耗竭期间出现的交感 - 肾上腺素能反应降低及肾素 - 血管紧张素系统的主导作用。
