Ehlenz K, Peter J H, Kaffarnik H, von Wichert P
Abt. Für Endokrinologie und Stoffwechsel, Abt. Poliklinik, Zentrum für Innere Medizin, Universität Marburg.
Pneumologie. 1991 May;45 Suppl 1:239-45.
Recent studies about renal function and volume regulating hormones in obstructive sleep apnea (oSAS) indicate complex disturbances in volume homeostasis. Increased nocturnal secretion of atrial natriuretic peptide (ANP) and decreased renin secretion during apnea looks similar to a situation seen during hypervolemia or increased cardiac volume load. Increased venous return induced by pathologically high negative intrathoracic pressure during obstructive apnea may be the cause. Since during wakefulness no true hypervolemia is present, a "pseudohypervolemia" or "central hypervolemia" must exist caused by volume shift from the peripheral to the central compartment during apnea. Since volume homeostasis and blood pressure regulation are complexly connected the question arises whether disturbances in volume homeostasis play a role in the pathogenesis of arterial hypertension in sleep apnea. In a subgroup of hypertensive patients hypertension is salt-sensitive and volume dependent; it is called volume-expanded or low-renin hypertension. An inhibitor of the Na+/K(+)-ATPase acting via the digitalis receptor - called digitalis like factor (DLF) - is regarded as the causative agent for the development of hypertension in these cases. From this background, we were interested in the question whether DLF may be the linkage between disturbances in volume homeostasis and the pathogenesis of hypertension in sleep apnea. We could demonstrate a decrease of nocturnal urinary excretion of DLF during nasal continuous positive air pressure (nCPAP) therapy. Since a positive correlation between changes in diuresis respectively natriuresis and DLF excretion was found, we suggested DLF to be involved in changes of renal function in sleep apnea besides ANP. In 3 patients we measured nocturnal plasma levels of DLF and renin.(ABSTRACT TRUNCATED AT 250 WORDS)
近期关于阻塞性睡眠呼吸暂停(OSAS)中肾功能和容量调节激素的研究表明,容量稳态存在复杂紊乱。呼吸暂停期间心房利钠肽(ANP)夜间分泌增加和肾素分泌减少,类似于血容量过多或心脏容量负荷增加时的情况。阻塞性呼吸暂停期间病理性高胸内负压引起的静脉回流增加可能是原因。由于清醒时不存在真正的血容量过多,呼吸暂停期间外周至中心腔室的容量转移必然导致“假性血容量过多”或“中枢性血容量过多”。由于容量稳态和血压调节密切相关,因此出现了容量稳态紊乱是否在睡眠呼吸暂停引起的动脉高血压发病机制中起作用的问题。在一部分高血压患者中,高血压对盐敏感且依赖容量;称为容量扩张性或低肾素性高血压。一种通过洋地黄受体起作用的Na+/K(+)-ATP酶抑制剂——称为洋地黄样因子(DLF)——被认为是这些病例中高血压发展的致病因素。基于此背景,我们对DLF是否可能是睡眠呼吸暂停中容量稳态紊乱与高血压发病机制之间的联系这一问题感兴趣。我们能够证明在经鼻持续气道正压通气(nCPAP)治疗期间,DLF的夜间尿排泄量减少。由于发现利尿和钠尿变化与DLF排泄之间存在正相关,我们认为除了ANP外,DLF也参与了睡眠呼吸暂停时的肾功能变化。我们对3例患者测量了夜间血浆中DLF和肾素的水平。(摘要截选至250词)