Nussdorfer G G, Mazzocchi G, Meneghelli V
Department of Anatomy, University of Padua, Italy.
Endocr Res. 1988;14(4):293-303. doi: 10.1080/07435808809032991.
Prolonged (12-day) sodium deprivation strikingly raised both basal plasma aldosterone concentration (PAC) (114%) and plasma renin activity (PRA) (200%), and lowered ANF blood level (-30%). Acute ANF bolus administration produced a dose-dependent decrease in PAC in both normally-fed and sodium-restricted rats. The maximum effect (-30/-37%) was observed with a dose of 20 micrograms.kg-1. The interruption of the renin-angiotensin system (RAS), obtained by a 7-day infusion of captopril and maintenance doses of angiotensin II, did not cause significant changes in PAC in animals kept on a normal diet, while it did induce a significant lowering of PAC in sodium-restricted rats (-25%). This treatment evoked in both groups of animals a notable reduction of PRA (-61/-89%). A 7-day infusion with ANF (at a rate of 20 micrograms.kg-1.h-1) notably lowered PAC (-32%) in normally-fed rats, independently of the RAS status. The same occurred in sodium-deprived rats, but the effect was more intense in animals with intact RAS (-41% vs -24%). Prolonged ANF infusion significantly reduced PRA (-48%) only in sodium-restricted rats with intact RAS. These findings suggest that (i) the long-term inhibitory effect of ANF on aldosterone secretion is due to both the block of renin release and a direct action on the zona glomerulosa; and (ii) the mechanism underlying the adrenoglomerulotrophic effect of sodium restriction involves not only the activation of RAS, but also the suppression of ANF release.
长期（12天）缺钠显著提高了基础血浆醛固酮浓度（PAC）（114%）和血浆肾素活性（PRA）（200%），并降低了心房钠尿肽血水平（-30%）。急性给予心房钠尿肽大剂量注射在正常喂养和限钠大鼠中均产生了剂量依赖性的PAC降低。在剂量为20微克·千克⁻¹时观察到最大效应（-30/-37%）。通过7天输注卡托普利和维持剂量的血管紧张素II来阻断肾素-血管紧张素系统（RAS），在正常饮食的动物中未引起PAC的显著变化，而在限钠大鼠中却导致PAC显著降低（-25%）。这种处理在两组动物中均引起了PRA的显著降低（-61/-89%）。以20微克·千克⁻¹·小时⁻¹的速率进行7天的心房钠尿肽输注，在正常喂养的大鼠中显著降低了PAC（-32%），与RAS状态无关。在缺钠大鼠中也出现了同样的情况，但在RAS完整的动物中效应更强（-41%对-24%）。仅在RAS完整的限钠大鼠中，长期输注心房钠尿肽显著降低了PRA（-48%）。这些发现表明：（i）心房钠尿肽对醛固酮分泌的长期抑制作用是由于肾素释放的阻断以及对球状带的直接作用；（ii）钠限制的肾上腺球状带营养作用的潜在机制不仅涉及RAS的激活，还涉及心房钠尿肽释放的抑制。
