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)