Pathogenesis of obstructive sleep apnoea in hypertensive patients: role of fluid retention and nocturnal rostral fluid shift.

Obstructive sleep apnoea (OSA) is highly prevalent in hypertensive patients, particularly those with drug resistance. Evidence from animal experiments, epidemiologic studies and clinical trials strongly suggest a causal link. Mechanistic studies argue for increased sympathetic neural activity and endothelial dysfunction. However, disturbances in fluid volume regulation and distribution may also be involved in the pathogenesis of these two conditions. Several studies have shown a high prevalence of OSA in fluid-retaining states including hypertension, a direct relationship between the severity of OSA and the volume of fluid displaced from the legs to the neck during sleep, and a decrease in upper airway cross-sectional area in response to graded lower body positive pressure. Treatments targeting fluid retention and redistribution, including diuretics, mineralocorticoid antagonists, exercise, and possibly renal denervation lower blood pressure and reduce the apnoea-hypopnoea index, a measure of OSA severity. From these observations, it has been postulated that during the daytime, excess fluid collects in the lower extremities due to gravity, and on lying down overnight is redistributed rostrally to the neck, where it may narrow the upper airway and increase its collapsibility, predisposing to OSA when pharyngeal dilator muscle activity decreases during sleep. This article discusses the associations between OSA and hypertension and reviews the evidence for fluid accumulation and its nocturnal rostral redistribution in the pathogenesis of OSA in hypertensive patients.

Light requirement for induction and continuous accumulation of an ammonium-inducible NADP-specific glutamate dehydrogenase in chlorella.

The ammonium-inducible NADP-specific glutamate dehydrogenase of Chlorella sorokiniana was shown to require light for both its induction by ammonia in uninduced cells, and its continuous accumulation in fully induced cells. Addition of ammonia to uninduced cells in the light resulted in a 35-minute induction lag followed by linear and coincident increases in enzyme activity and antigen. Enzyme activity was not induced in the dark; however, transfer of these cells to the light resulted in an immediate increase in enzyme activity and antigen. The absence of an induction lag suggested that mRNA sequences and/or an enzyme precursor with different antigenic properties than the active holoenzyme accumulated in cells in the dark in ammonium medium. When fully induced cells were transferred to the dark, the activity of the enzyme quickly ceased to accumulate. In contrast to the NADP-specific isozyme, the cells also contain a constitutive NAD-specific isozyme which was shown to accumulate in cells in the dark in either ammonium or nitrate medium.