Farese R V, Rodriguez-Colomé M, O'Malley B C
Clin Endocrinol (Oxf). 1980 Nov;13(5):447-53. doi: 10.1111/j.1365-2265.1980.tb03410.x.
Urinary immunoreactive PGA and PGE, plasma and urinary aldosterone, and plasma renin activity (PRA) were determined in eleven control subjects and four patients with diabetic hyporeninaemic hypoaldosteronism (HH) before and during 4 days of sodium chloride restriction and frusemide administration. Aldosterone and PRA increased steadily in control subjects, but not in patients with HH. Increases in urinary PGA and PGE were observed during volume depletion. The basal levels and increases observed were comparable in both groups. The apparently normal stimulation of PGA and PGE in subjects with diabetic HH suggests that this syndrome is not associated with abnormal prostaglandin metabolism, despite the fact that drug-induced abnormalities of the latter may precipitate or aggravate the clinical syndrome in susceptible individuals. The increase in PGA and PGE following frusemide treatment and salt depletion supports the possibility of a relationship between renal prostaglandin metabolism, frusemide-induced natriuresis and/or renin secretion. While the nature of this relationship remains obscure, the increases in PGA and PGE in the absence of increases in renin-angiotensin levels in subjects with HH suggests that these changes are not due to activation of the renin-angiotensin system.
在11名对照受试者和4名糖尿病低肾素性低醛固酮血症（HH）患者中，于氯化钠限制和服用速尿4天之前及期间，测定了尿免疫反应性PGA和PGE、血浆和尿醛固酮以及血浆肾素活性（PRA）。对照受试者的醛固酮和PRA稳步升高，但HH患者未出现这种情况。在容量耗竭期间观察到尿PGA和PGE升高。两组观察到的基础水平及升高情况具有可比性。糖尿病HH患者中PGA和PGE的刺激明显正常，这表明尽管药物诱导的前列腺素代谢异常可能在易感个体中引发或加重临床综合征，但该综合征与前列腺素代谢异常无关。速尿治疗和盐耗竭后PGA和PGE的升高支持了肾前列腺素代谢、速尿诱导的利钠作用和/或肾素分泌之间存在关联的可能性。虽然这种关系的性质仍不清楚，但HH患者中PGA和PGE升高而肾素 - 血管紧张素水平未升高表明这些变化并非由于肾素 - 血管紧张素系统的激活。
