Weidmann P, Matter D R, Matter E E, Gnädinger M P, Uehlinger D E, Shaw S, Hess C
Medizinische Poliklinik, University of Bern, Switzerland.
J Clin Endocrinol Metab. 1988 Jun;66(6):1233-9. doi: 10.1210/jcem-66-6-1233.
To investigate the influence of a mineralocorticoid and a glucocorticoid on plasma immunoreactive atrial natriuretic peptide (irANP) and possible functional correlates, eight normal men received in random order 9 alpha-fludrocortisone acetate (9 alpha F; 0.6 mg/day), prednisone (50 mg/day), and placebo each for 9 days. Their diet contained 130 mmol sodium and 75 mmol potassium daily. The mean supine plasma irANP levels were similar on days 2, 4, and 9 of placebo treatment [25 +/- 10 (+/- SE), 27 +/- 5, and 27 +/- 6 pmol/L, respectively]. Mean plasma irANP levels were 76 +/- 42 (P less than 0.05), 89 +/- 34, and 93 +/- 29 pmol/L (P less than 0.01), respectively, on days 2, 4, and 9 during 9 alpha F administration, and 68 +/- 37 (P less than 0.05), 83 +/- 41, and 48 +/- 18 pmol/L on the same days during prednisone administration. Compared with the placebo period, sodium intake minus urinary output during 9 alpha F administration averaged +41 mmol at the time of blood sampling on day 2, +112 mmol on day 4, and +149 mmol on day 9; body weight was unchanged on day 2 and increased by 0.7 and 1.1 kg on days 4 and 9, respectively. Escape from 9 alpha F-induced renal sodium retention occurred on days 5 and 6. During prednisone administration, sodium intake minus urinary output and body weight did not change. Plasma volume and BP rose significantly during 9 alpha F (P less than 0.05) but not during prednisone administration. Plasma renin, aldosterone, and norepinephrine (NE) decreased during 9 alpha F treatment (P less than 0.05 to less than 0.01); during prednisone treatment, plasma aldosterone levels were lower on day 9 only. Cardiovascular pressor responsiveness to angiotensin II was enhanced during 9 alpha F but not prednisone administration, while blood pressure reactivity to NE was not significantly modified. These findings demonstrate that 9 alpha F and prednisone in high doses provoke remarkably similar increases in plasma irANP, but that the glucocorticoid-induced rise in plasma irANP is due to a mechanism other than sodium and volume retention.
为研究盐皮质激素和糖皮质激素对血浆免疫反应性心房钠尿肽（irANP）的影响及其可能的功能关联，8名正常男性按随机顺序分别接受9α-氟氢可的松醋酸酯（9αF；0.6毫克/天）、泼尼松（50毫克/天）及安慰剂治疗，各为期9天。他们的日常饮食中每日含130毫摩尔钠和75毫摩尔钾。安慰剂治疗的第2、4和9天，平均仰卧位血浆irANP水平相似[分别为25±10（±标准误）、27±5和27±6皮摩尔/升]。在给予9αF期间，第2、4和9天的平均血浆irANP水平分别为76±42（P<0.05）、89±34和93±29皮摩尔/升（P<0.01）；在给予泼尼松期间，相同日期的平均血浆irANP水平分别为68±37（P<0.05）、83±41和48±18皮摩尔/升。与安慰剂期相比，给予9αF期间，在第2天采血时钠摄入量减去尿量平均增加41毫摩尔，第4天增加112毫摩尔，第9天增加149毫摩尔；第2天体重未变，第4天和第9天分别增加0.7千克和1.1千克。9αF诱导的肾钠潴留于第5天和第6天出现逃逸现象。给予泼尼松期间，钠摄入量减去尿量及体重均未改变。给予9αF期间血浆容量和血压显著升高（P<0.05），而给予泼尼松期间则无此现象。给予9αF治疗期间血浆肾素、醛固酮和去甲肾上腺素（NE）降低（P<0.05至<0.01）；给予泼尼松治疗期间，仅第9天血浆醛固酮水平降低。给予9αF期间心血管对血管紧张素II的升压反应增强，而给予泼尼松期间则无此现象，同时血压对NE的反应性无明显改变。这些发现表明，高剂量的9αF和泼尼松可使血浆irANP显著升高且二者相似，但糖皮质激素诱导的血浆irANP升高是由钠潴留和容量潴留以外的机制所致。
