Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart rate variability (HRV) has become a useful parameter for the quantification of autonomic nervous function. HRV has been quantified, either by time domain or frequency domain analysis. Time domain measures, such as CVRR and RR50, are easy to calculate but they only provide information related to parasympathetic activity. The spectral analyses, on the other hand, give us information concerning 3 oscillatory components. The high frequency band (the frequency between 0.15-0.5 Hz) is known as the respiratory sinus arrhythmia (RSA), and the middle frequency band (0.88-0.15 Hz) is attributed to baroreflex components. The low frequency band (0.01-0.08 Hz) may be of various origins, such as blood flow rhythm, periodic respiration (including Cheyne-Stokes respiration), renin-angiotensin, and thermal regulation. The efferent nerve to the high frequency band is totally operated by the parasympathetic system. The low frequency band is regulated by both sympathetic and parasympathetic nervous systems. We demonstrated that the diurnal variation of HRV may afford additional information, such as ultradian changes of autonomic activity, possibly due to REM/NREM cycles. It is believed that simultaneous monitoring of other physiological parameters such as EEG, EOG, respiration, and blood pressures, might give us information concerning the dynamic nature of autonomic nervous function.
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PMID:[Heart rate variability]. 161 51

This study examined the relationship between aldosterone secretion and sleep stages in conjunction with two aldosterone regulating hormone systems, the renin-angiotensin system (RAS) and adrenocorticotropin (ACTH), and also K+. Nocturnal plasma patterns of aldosterone, plasma renin activity (PRA), ACTH and K+ were established in blood collected at 10-min intervals in two groups of 6 subjects. Both groups underwent two 9 hour overnight-studies, consisting of one control night and one experimental night. The first group was maintained on a low Na diet and the other was given a beta-blocker, atenolol. Polygraphic recordings of sleep were scored according to established criteria. For the control night, REM sleep usually began at peak level or in the descending phase of aldosterone oscillations. As previously described, PRA reflected REM-NREM sleep alteration, levels increased in NREM and decreased during REM sleep. ACTH fluctuations did not oscillate with sleep stages, but levels were very seldom in the ascending phase at REM sleep onset. Plasma K+ remained almost constant throughout the night. The relative importance of the ACTH and the RAS on nocturnal aldosterone secretion and the relationship between aldosterone oscillations and sleep stages remained unclear. Modulating renin levels by either consuming a low Na diet or administration of a beta-blocker enabled this relationship to be clarified. The RAS dominated aldosterone secretion when stimulated by a low sodium diet. Aldosterone oscillations then reflected PRA oscillations with a delay of about 20 min and the relationship of aldosterone to sleep stages was dependent on the relationship of PRA with sleep stages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nocturnal oscillations of plasma aldosterone in relation to sleep stages. 196 35

In previous studies, we established a strong concordance between nocturnal oscillations in plasma renin activity (PRA) and REM-NREM sleep cycles. To determine whether this relation persists in the case of moderate essential hypertension and if it is influenced by antihypertensive therapies affecting renin release, six normal subjects and six hypertensive patients were studied. The normal subjects underwent one control night. The hypertensive patients were studied during a first night when a placebo was given. Four of them underwent a second night following a single dose of an angiotensin-converting enzyme (ACE) inhibitor, perindopril; and a third night, 45 days later, with the antihypertensive treatment. In addition, two of the patients underwent two night-studies, after a single and repeated doses of a beta-blocker, atenolol, to see whether preventing renin release modified the sleep structure. The relationship between the nocturnal PRA oscillations and the sleep stage patterns persisted in hypertensive patients receiving placebo. In patients who had low PRA levels, the increases associated with NREM sleep were small. However, the mean relative amplitude of the oscillations, expressed as a percentage of the nocturnal mean, was about 60%, which was similar to that in normotensive subjects. Active renin and PRA oscillations were closely coupled. ACE activity profiles displayed damped fluctuations and no systematic relationship with sleep stages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nocturnal oscillations in plasma renin activity during sleep in hypertensive patients: the influence of perindopril. 217 56

To establish the strength of the relationship between the nocturnal oscillations in plasma renin activity (PRA) and the sleep stage patterns, 42 PRA profiles from blood collected at 10-min intervals and the concomitant polygraphic sleep recordings were analyzed. In all cases, PRA curves exactly reflected the pattern of sleep stage distribution. When sleep cycles were complete, PRA levels oscillated at a regular 100-min period, with a strong spectral density. Declining PRA levels always coincided with REM sleep phases and increasing levels with NREM sleep phases. More precisely, peak levels corresponded to the transition from deep sleep stages toward lighter ones. The start of the rises in PRA generally marked the transition from REM sleep to stage 2. For incomplete sleep cycles, PRA curves reflected all disturbances and irregularities in the sleep structure. Spontaneous and provoked awakenings blunted the rise in PRA normally associated with NREM sleep, which indicates that disturbing sleep modifies the renin release from the kidneys. These results suggest that a common mechanism within the central nervous system controls both PRA oscillations and the REM-NREM sleep alternation.
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PMID:Nocturnal oscillations in plasma renin activity and REM-NREM sleep cycles in humans: a common regulatory mechanism? 304 38

During night-sleep, plasma renin activity displays periodic oscillations which are closely related to the alternation of REM-NREM sleep. To see whether this nocturnal rhythm persisted during the day-time, plasma renin activity was measured every 10 min for 24 hours in 4 human volunteers and in 4 others over a 10-h day-time period. To avoid the influence of repeated food intake which stimulates renin release, the subjects were on continuous enteral nutrition. Spectral analyses of the data revealed clear differences between the nocturnal and the diurnal PRA patterns. In subjects on enteral nutrition, sustained 100-min oscillations with strong spectral densities persisted during the night. They were closely related to REM-NREM cycles. During the day-time, however, the fluctuations were damped and less regular, and power spectra were split into 2 or 3 peaks without any predominant period. These results demonstrate that regular 100-min PRA oscillations could only be detected during night-sleep. The clear night-day differences suggest that the underlying oscillatory mechanisms may be weaker during day-time or may be counteracted by other physiological processes.
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PMID:Night-day differences in the ultradian rhythmicity of plasma renin activity. 310 99

The aim of the present study was to investigate changes in blood pressure, heart rate, renal plasma flow, catecholamines, renin and angiotensin in fifteen patients with uncomplicated essential hypertension. During sleep a progressive fall in blood pressure and heart rate was found. Renal plasma flow and calculated renal vascular resistance were reduced as well. Noradrenaline and adrenaline decreased, but renin and angiotensin rose. The rise in renin was inversely related to age. Blood pressure was more variable during REM-sleep but otherwise there were no differences in the level of blood pressure and catecholamines during REM-sleep or during sleep stage IV.
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PMID:Effect of sleep on blood pressure and its correlates. 389 Nov 52

Diurnal studies were performed on ten normal volunteers taking a normal sodium diet. Half-hourly blood samples were taken throughout 25 h and assayed for plasma renin activity (PRA) and the plasma concentrations of noradrenaline, aldosterone and cortisol. Sleep was recorded polygraphically and scored by standard criteria. Circadian rhythms were demonstrated for plasma cortisol, aldosterone and noradrenaline concentrations, but not for plasma renin activity. The nadir of the rhythm for the noradrenaline concentration appeared to be related to sleep itself rather than to any chronological index. Only PRA was effected by the stage of sleep, falling sharply during periods of REM sleep. Plasma cortisol and aldosterone concentrations showed a positive correlation over the 24 h. There was, however, no correlation between PRA and plasma aldosterone concentrations, except when the subjects arose after their night's recumbency. Plasma noradrenaline concentration did not correlate with the concentration of any of the other hormones measured.
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PMID:Studies of diurnal changes in plasma renin activity, and plasma noradrenaline, aldosterone and cortisol concentrations in man. 702 Oct 8

Even if different mechanisms of various interactions during sleep are known, it is still unsolved by which mechanisms physiological reactions during sleep may start a pathophysiological course. Hypoxia, Hypercapnia and repetitive sympathetic elevations are well known elements in the control of the arterial resistance. Furthermore investigations in patients with sleep apnea showed changes of the pulsatile secretion pattern within the renin-angiotensin-system and the antinatriuretic peptides. These changes were reversible under nasal CPAP-therapy, nycturia as a frequent symptom disappeared. Nevertheless neither hypoxia nor intrathoracic pressure changes nor the arousals can assert the longterm influence on the blood pressure alone, a multifactorial confluence must be assumed. Further it is unclear how a tonic increase of the arterial blood pressure may occur in dependence of the REM- and NREM-sleep cycle changes as well as during daytime. First investigations in sleeping man seem to indicate, that a disturbance of the physiological coupling of breathing and circulation may present a pathogenetic element. Finally it remains open, whether the changes of the cardiorespiratory coupling during sleep of control persons and of patients with OSA are comparable, and whether they may be procured for an explanation of the pathogenesis of arterial and pulmonary hypertension. Further investigations in the control mechanisms of breathing and circulation related to the circuits of chemo- and baroreception, thresholds during wakefulness and sleep may be of decisive help to process the question, to what extent clinical states find a correlate in a disturbed cardiorespiratory coupling and, much more significantly, whether a disturbance in the physiological cardiorespiratory coupling appears already in early states of a disease. Sleep with ist complex physiology as well as with its characteristic pathophysiological phenomenon of sleep related breathing disorders has opened a new interdisciplinary field where tools like the polysomnography and electronic data analysis are used by physiologists, pathophysiologists as well as by physicians.
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PMID:[Cardiorespiratory coupling in obstructive sleep apnea (OSA)]. 924 90

Similar periodicities of about 90-100 min characterize both hormone pulsatility and NREM-REM sleep cycles suggesting that both processes could be temporally linked. From the current knowledge of the literature, it appears that, in spite of the diversity of the relationship between hormones and the sleep/wake cycle, systematic relationships exist between hormone pulses and the NREM-REM sleep cycles. Early studies have demonstrated the temporal association between GH and SWS episodes occurring soon after sleep onset. Renin, a key enzyme of the renin-angiotensin system, displays nocturnal oscillations that are associated strongly with the NREM-REM sleep cycles, and represents the first identified biological marker of sleep stage alternation. SWS invariably occurs in the descending phases of TSH and cortisol pulses which suggests that some specific mechanisms of this sleep stage could modulate their levels or, conversely, that increased TSH and cortisol secretion prevents the occurrence of deep sleep. Apart from the period of sleep onset associated with reduced prolactin secretion, no systematic relationship has been found between REM sleep and hormone release. These results highlight the complexity of hormone and sleep interactions and provide a basis for further research into their functional significance.
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PMID:Symposium: Normal and abnormal rem sleep regulation: Episodic hormone release in relation to REM sleep. 1060 94

Spectral analysis of heart rate variability (HRV) during overnight polygraphic recording was performed in 11 healthy subjects. The total spectrum power, power of the VLF, LF and HF spectral bands and the mean R-R were evaluated. Compared to Stage 2 and Stage 4 non-REM sleep, the total spectrum power was significantly higher in REM sleep and its value gradually increased in the course of each REM cycle. The value of the VLF component (reflects slow regulatory mechanisms, e.g. the renin-angiotensin system, thermoregulation) was significantly higher in REM sleep than in Stage 2 and Stage 4 of non-REM sleep. The LF spectral component (linked to the sympathetic modulation) was significantly higher in REM sleep than in Stage 2 and Stage 4 non-REM sleep. On the contrary, a power of the HF spectral band (related to parasympathetic activity) was significantly higher in Stage 2 and Stage 4 non-REM than in REM sleep. The LF/HF ratio, which reflects the sympathovagal balance, had its maximal value during REM sleep and a minimal value in synchronous sleep. The LF/HF ratio significantly increased during 5-min segments of Stage 2 non-REM sleep immediately preceding REM sleep compared to 5-min segments of Stage 2 non-REM sleep preceding the slow-wave sleep. This expresses the sympathovagal shift to sympathetic predominance occurring before the onset of REM sleep. A significant lengthening of the R-R interval during subsequent cycles of Stage 2 non-REM sleep was documented, which is probably related to the shift of sympathovagal balance to a prevailing parasympathetic influence in the course of sleep. This finding corresponds to a trend of a gradual decrease of the LF/HF ratio in subsequent cycles of Stage 2 non-REM sleep.
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PMID:Spectral analysis of the heart rate variability in sleep. 1558 54


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