Partial characterization of a renin-releasing factor from plasma and hypothalamus.

Kar, Louis D. Van de; Urban, Janice H.; Brownfield, Mark S.; Simmons, W H

doi:10.1161/01.hyp.9.6.598

Cited by 19 publications

(15 citation statements)

References 25 publications

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“…Subsequently, delta wave activity increased within 10±20 min and was associated with a lag of 0±10 min with an increase in PRA. These results suggest that pressure-dependent mechanisms are involved in the generation of nocturnal PRA oscillations rather than sleep-related mechanisms, possibly involving serotoninergic pathways (Rittenhouse et al 1992; Van de Kar et al 1981, 1987, as previously hypothesized (Brandenberger et al 1990). These ®ndings imply that there is probably no need for evoking common central mechanism increasing both slow wave activity and renin release from the kidneys.…”

Section: Discussionsupporting

confidence: 59%

“…In patients with sleep disorders, PRA variations re¯ect the internal sleep structure disorganization (Brandenberger et al 1996;Follenius et al 1991). These ®ndings suggest that common central mechanisms, possibly involving the serotoninergic system (Rittenhouse et al 1992; Van de Kar et al 1981, 1987, control both the alternation of the sleep stages and renin release from the juxtaglomerular cells. However, previous studies have reported a reduction in averaged blood pressure levels during NREM sleep and a high variability with a slight enhancement during REM sleep (Khatri and Freis 1966;Snyder et al 1964).…”

Section: Introductionmentioning

confidence: 96%

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

Charloux¹,

Piquard²,

Ehrhart³

et al. 2002

Journal of Sleep Research

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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.

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Section: Discussionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 96%

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

Charloux¹,

Piquard²,

Ehrhart³

et al. 2002

Journal of Sleep Research

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“…A possible role for serotonin, which is involved both in sleep during waking periods, when serotonin discharge is high, does not support this hypothesis. 24 A possible role for the renin-releasing peptide recently characterized by Van de Kar et al 25 must await further investigation. However, it may well prove difficult to isolate one single factor from the multiple processes underlying sleep stage alternation.…”

Section: Subjects Receiving Atenololmentioning

confidence: 98%

Modulation of episodic renin release during sleep in humans.

Brandenberger¹,

Krauth²,

Ehrhart³

et al. 1990

Hypertension

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We previously described a strong concordance between nocturnal oscillations in plasma renin activity and sleep cycles. To examine whether modifying renal renin content or release influences the response to central stimuli linked to sleep stage alternation, plasma renin activity was measured every 10 minutes from 11:00 PM to 8:00 AM in three groups of six subjects. The first group received one 40 mg dose of the diuretic furosemide; the second group underwent the night experiment after 3 days on a low sodium diet; the third group received one 100 mg dose of the 0-blocker atenolol. Each subject underwent a control night when a placebo was given. The nocturnal curves were analyzed with a pulse detection program. For the control nights, 74 of the 83 sleep cycles were associated with significant plasma renin activity oscillations; non-rapid eye movement sleep occurred in the ascending portions and rapid eye movement sleep in the declining portions of the oscillations. These oscillations persisted in the three groups of subjects during the experimental nights and the relation with the sleep stages was not disturbed. Acute stimulation by furosemide amplified the oscillations and led to a general upward trend of the nocturnal profiles. Similarly, a low sodium diet, which led to a slow increase in renal renin content, provoked large oscillations with high initial levels. However, in both cases the mean relative amplitude of the oscillations, expressed as a percentage of the nocturnal means, was similar to that of the control nights and approximated 60%. Atenolol reduced the increases associated with non-rapid eye movement sleep. Small oscillations were detected in 16 of the 23 sleep cycles recorded. These results give evidence of the strength of the sleep-related processes generating the oscillations, which are amplified or depressed by factors known to control renin release. These factors create a baseline environment that modulates the expression of central stimuli associated to the transition from rapid eye movement sleep or waking period toward deep sleep stages. {Hypertension 1990;15:370-375)

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“…Discrete cellselective lesions have shown that this increase in PRA is mediated by neurons in the paraventricular nucleus of the hypothalamus (24). A renin-releasing factor, which is probably a peptide, has been partially characterized from rat plasma and hypothalamus (25). The role of the serotoninergic system in renin secretion during sleep has not yet been confirmed in humans.…”

Section: Discussionmentioning

confidence: 99%

Oscillations in Sympatho-Vagal Balance Oppose Variations inδ -Wave Activity and the Associated Renin Release

Charloux¹,

Otzenberger²,

Gronfier³

et al. 1998

The Journal of Clinical Endocrinology & Metabolism

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To determine the potential role of the sympathetic nervous system in the generation of the oscillations in PRA over the 24-h period, we used the autocorrelation coefficient of RR interval (rRR), a new tool to evaluate the sympatho-vagal balance continuously. We determined the influence of the sympathetic nervous system both on the nocturnal PRA oscillations associated to increases in ␦-wave activity and on the daytime oscillations that occur randomly in awake subjects.PRA and rRR were determined every 10 min during 24 h in nine healthy subjects under continuous bed rest. Electroencephalographic spectral analysis was used to establish the variations in ␦-wave activity during sleep, from 2300 -0700 h. The overnight profiles in PRA, rRR, and ␦-wave activity were analyzed using a modified version of the pulse detection program ULTRA. The temporal link among the profiles of rRR, PRA, and ␦-wave activity was quantified using crosscorrelation analysis.During sleep, large oscillations in PRA were strongly linked to variations in ␦-wave activity. They were preceded by opposite oscillations in rRR, decreases in rRR reflecting predominant vagal activity, and increases in rRR reflecting sympathetic dominance. During the waking periods, the levels of rRR were higher, with smaller variations. The daytime PRA oscillations were not associated with any significant changes in rRR, and conversely, significant oscillations in rRR were not followed by any significant changes in PRA.In conclusion, the sympathetic nervous system is not directly involved in the generation of renin oscillations observed under basal conditions. During sleep, the oscillations in sympatho-vagal balance are inversely related to the variations in ␦-wave activity and the associated renin release. The processes that give the intermittent signal for concomitant increases in slow wave activity and renin release from the kidney remain to be identified. (J Clin Endocrinol

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Partial characterization of a renin-releasing factor from plasma and hypothalamus.

Cited by 19 publications

References 25 publications

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

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

Modulation of episodic renin release during sleep in humans.

Oscillations in Sympatho-Vagal Balance Oppose Variations inδ -Wave Activity and the Associated Renin Release

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