Naess P A, Bugge J F, Christensen G
Institute for Experimental Medical Research, University of Oslo, Ullevål Hospital, Norway.
Scand J Clin Lab Invest. 1996 Nov;56(7):665-70. doi: 10.1080/00365519609090603.
To examine the effect of atrial natriuretic factor (ANF) on renin release induced by renal hypotension, experiments were performed in seven barbiturateanaesthetized dogs with denervated kidneys. Renin release induced by renal arterial constriction to 55 mmHg was measured before and during intrarenal infusion of ANF (200 ng min-1 kg-1 body weight). Before ANF infusion, renal arterial constriction increased renin release from 0.2 +/- 0.1 to 21.8 +/- 3.3 micrograms angiotensin I min-1 (p < 0.05). During ANF infusion renal arterial constriction increased renin release as much as before from 0.8 +/- 0.6 to 23.7 +/- 4.6 micrograms angiotensin I min-1 (p < 0.05). Although ANF increased glomerular filtration rate from 33.9 +/- 4.2 to 43.4 +/- 5.6 ml min-1 (p < 0.05) and sodium excretion from 72 +/- 22 to 567 +/- 112 mumol min-1 (p < 0.05) at normal renal perfusion pressure, ANF was without effect on glomerular filtration rate and sodium excretion during renal arterial constriction. The present study shows that ANF is not an inhibitor of renin release induced by renal arterial constriction in anaesthetized dogs with denervated kidneys. Our findings indicate that ANF does not influence renin release induced by the haemodynamic mechanism.
为研究心房利钠因子（ANF）对肾性低血压诱导的肾素释放的影响，在7只去神经支配肾脏的巴比妥类麻醉犬身上进行了实验。在肾内输注ANF（200 ng·min⁻¹·kg⁻¹体重）之前和期间，测量肾动脉收缩至55 mmHg时诱导的肾素释放。在输注ANF之前，肾动脉收缩使肾素释放从0.2±0.1增加至21.8±3.3微克血管紧张素I·min⁻¹（p<0.05）。在输注ANF期间，肾动脉收缩使肾素释放增加程度与之前相同，从0.8±0.6增加至23.7±4.6微克血管紧张素I·min⁻¹（p<0.05）。尽管在正常肾灌注压下，ANF使肾小球滤过率从33.9±4.2增加至43.4±5.6 ml·min⁻¹（p<0.05），钠排泄从72±22增加至567±112 μmol·min⁻¹（p<0.05），但在肾动脉收缩期间，ANF对肾小球滤过率和钠排泄无影响。本研究表明，在去神经支配肾脏的麻醉犬中，ANF不是肾动脉收缩诱导的肾素释放的抑制剂。我们的研究结果表明，ANF不影响血流动力学机制诱导的肾素释放。
