Time‐courses in renin and blood pressure during sleep in humans

Abstract

SUMMARY We previously described a strong concordance between nocturnal oscillations in plasma renin activity (PRA) and the rapid eye movement (REM) and non-REM (NREM) sleep cycles, but the mechanisms inducing PRA oscillations remain to be identi®ed. This study was designed to examine whether they are linked to sleep stage-related changes in arterial blood pressure (ABP). Analysis of sleep electroencephalographic (EEG) activity in the delta frequency band, intra-arterial pressure, and PRA measured every 10 min was performed in eight healthy subjects. Simultaneously, the ratio of low frequency power to low frequency power + high frequency power [LF/(LF + HF)] was calculated using spectral analysis of R±R intervals. The cascade of physiological events that led to increased renin release during NREM sleep could be characterized. First, the LF/(LF + HF) ratio signi®cantly (P < 10 A4 ) decreased, indicating a reduction in sympathetic tone, concomitantly to a signi®cant (P < 10 A3 ) decrease in mean arterial pressure (MAP). Delta wave activity increased (P < 10 A4 ) 10±20 min later and was associated with a lag of 0±10 min with a signi®cant rise in PRA (P < 10 A4 ). Rapid eye movement sleep was characterized by a signi®cant increase (P < 10 A4 ) in the LF/(LF + HF) ratio and a decrease (P < 10 A4 ) in delta wave activity and PRA, whereas MAP levels were highly variable. Overnight cross-correlation analysis revealed that MAP was inversely correlated with delta wave activity and with PRA (P < 0.01 in all subjects but one). These results suggest that pressure-dependent mechanisms elicit the nocturnal PRA oscillations rather than common central processes controlling both the generation of slow waves and the release of renin from the kidney.

Sleep deprivation induces excess diuresis and natriuresis in healthy children

“…The modulation of RAAS found in this study might be secondary to changes in blood pressure although previous reports have found a close relationship between renin secretion and sleep stages with increased renin levels during REM stages (4). The same group later reported that changes in sympathetic tone during sleep leading to MAP reduction preceded the increase in renin, pointing toward pressure-related changes rather than a central effect of sleep (5). We find that nonsleep increases blood pressure and decreases RAAS hormone levels.…”

Volume regulating hormone responses to repeated head-up tilt and lower body negative pressure

“…Although 70° HUT and −55 mmHg LBNP show similar cardiovascular responses and lead to similar amounts (approximately 600 mL) of venous pooling in the legs [15], endocrine effects of these stressors may be different because splanchnic pooling increases with passive head‐up tilt and drops during LBNP. This might explain a slight drop in mean arterial pressure with LBNP, possibly compensated for by a greater increase in PRA [20] compared with HUT, where arterial pressure increases, thereby lessening the magnitude of the reflex PRA response. It has been observed previously that graded doses of ACTH infusion lead to a linear increase in plasma aldosterone without changes in plasma sodium, potassium or PRA [21].…”

Sleep Disturbances as Nontraditional Risk Factors for Development and Progression of CKD: Review of the Evidence

“…28–31 As described above, normal sleep is accompanied by the so-called “dipping” of systolic and diastolic BP. A study by Charloux et al 29 that continuously recordedthe arterial BP of healthy volunteers using PSG identified this decrease in BP as the event that initiates a robust nocturnal elevation of plasma renin activity (PRA). Once sleep is initiated, sympatho-vagal balance is exquisitely modulated by the NREM-REM cycle, which is best quantified by assessing oscillations of EEG slow-wave activity using spectral analysis (Figure 2).…”