Disturbances in volume regulating hormone system--a key to the pathogenesis of hypertension in obstructive sleep apnea syndrome?
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)
Ehlenz
K
K
Abt. Für Endokrinologie und Stoffwechsel, Abt. Poliklinik, Zentrum für Innere Medizin, Universität Marburg.
Peter
J H
JH
Kaffarnik
H
H
von Wichert
P
P
D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001798:Blood Proteins / Q000494:pharmacology; D002298:Cardenolides; D004077:Digoxin; D004231:Diuresis; D006706:Homeostasis; D006801:Humans; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology; D009318:Natriuresis; D010953:Plasma Volume / Q000187:drug effects* / Q000502:physiology; D012083:Renin / Q000494:pharmacology*; D012503:Saponins; D012891:Sleep Apnea Syndromes / Q000503:physiopathology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000494:pharmacology
D001798:Blood Proteins; D002298:Cardenolides; D012503:Saponins; C034504:digoxin-like factors; D004077:Digoxin; D009320:Atrial Natriuretic Factor; D012083:Renin; D000254:Sodium-Potassium-Exchanging ATPase