Twenty-four-hour profiles of plasma renin activity in relation to the sleep-wake cycle

Brandenberger, G.; Follénius, M.; Goichot, B.; Saini, J.; Spiegel, Karine; Ehrhart, J; Simon, Chantal

doi:10.1097/00004872-199403000-00009

Cited by 99 publications

(67 citation statements)

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“…A possible reason for this result is the activation of the renin-angiotensin system at night and early morning. [36][37][38][39][40] To confirm this, it will be necessary to measure the UACR in a future study using fractional urine by a method such as the collection of urine every 2 hours. Regarding our biomarker investigation, we propose that bedtime administration of a telmisartan/amlodipine combination may reduce the risk of AF recurrence in hypertensive patients with paroxysmal AF, and a larger-scale randomized controlled study with the primary endpoint of AF recurrence is thus needed.…”

Section: Discussionmentioning

confidence: 99%

Dose Timing of an Angiotensin II Receptor Blocker/Calcium Channel Blocker Combination in Hypertensive Patients With Paroxysmal Atrial Fibrillation

Kario

Uchiyama²,

Yoshida³

et al. 2016

J of Clinical Hypertension

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It has long been thought that there is a close association between hypertension and atrial fibrillation (AF). However, the efficacy of an angiotensin II receptor blocker for the prevention of organ damage in hypertensive individuals with AF is still controversial. The present study was a multicentered, prospective, randomized, open-label clinical trial investigating the differences in the effect of treatment with telmisartan/amlodipine combination tablets on blood pressure (BP) levels and BP variability between morning and bedtime administration in hypertensive patients with paroxysmal AF, using ambulatory BP monitoring (ABPM) and home BP. With this treatment, the patients' 24-hour BP, nighttime BP, preawake BP, and morning BP shown by ABPM were significantly reduced, and the antihypertensive effects were similar regardless of the timing of the drug administration. The standard deviation of day-by-day home systolic BP and the maximum home systolic BP were also significantly reduced, and these effects were similar regardless of the treatment timing. The N-terminal pro-brain natriuretic peptide level was significantly decreased only in the bedtime administration group. A larger study will demonstrate whether the bedtime administration of telmisartan/amlodipine combination tablets maximizes the risklowering effect against AF recurrence in paroxysmal AF hypertensive patients. J Clin Hypertens (Greenwich). 2016;18:1036-1044. ª 2016 Wiley Periodicals, Inc.A close association between hypertension and atrial fibrillation (AF) has long been suspected. The Framingham Heart Study 1 showed that hypertension was an independent risk factor for incident AF in a general population, and uncontrolled elevated blood pressure (BP) was associated with an increased risk of incident AF in patients treated for hypertension.2 Based on overseas clinical trials, the main etiology of AF is hypertension in approximately 60% of AF patients.3 In addition, the Suita Study, 4 a cohort study in Japan, showed that hypertension was associated with an increased risk of incident AF.It is also suspected that hypertension not only facilitates the onset and persistence of AF, but also raises the risk of a thromboembolism. Antihypertensive treatment is therefore considered essential for hypertensive individuals with AF to prevent recurrent AF, cerebral infarction, or heart failure. 5 In several countries, angiotensin II receptor blockers (ARBs) have attracted attention as a therapeutic drug for hypertensive individuals with AF.6-9 However, the Atrial Fibrillation Clopidogrel Trial With Irbesartan for Prevention of Vascular Events (ACTIVE I) 10 comparing the effect of irbesartan on patients with AF (mainly persistent and permanent types) with that of placebo showed no differences between irbesartan and placebo for the recurrence of AF, indicating that ARBs did not suppress the recurrence of AF. Valsartan also did not reduce the recurrent AF rate in the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Atrial Fibrillation (GISSI-AF...

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Section: Discussionmentioning

confidence: 99%

Dose Timing of an Angiotensin II Receptor Blocker/Calcium Channel Blocker Combination in Hypertensive Patients With Paroxysmal Atrial Fibrillation

Kario

Uchiyama²,

Yoshida³

et al. 2016

J of Clinical Hypertension

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“…This is the opposite of the circadian pattern of normotensive rodents and humans, where the contribution of the RAS to BP is lower during the awake period and greater during sleep. 17,18 The reversed renin pattern is a likely additional factor besides the overall greater SNS activity in contributing in part to the hypertension in BPH/2J mice. The mechanism could possibly involve renal hyperinnervation, as well as enhanced sympathetically induced renin synthesis mediated by a diminution in miR-181a, a negative posttranscriptional regulator of Ren1 mRNA.…”

Section: Discussionmentioning

confidence: 99%

“…Plasma renin activity is normally elevated during sleep and reduced during the awake period. 18 Although renal Ren1 mRNA abundance was comparable between strains during the inactive period, levels were elevated during the active period in BPH/2J mice. This finding provides an explanation for the lack of differential expression of Ren1 mRNA in a prior transcriptomewide array study 6 and also for the similar renin expression demonstrated previously in the kidney of BPH/2J and BPN/3J mice.…”

Section: Contribution Of Ras To Hypertension In Bph/2j Micementioning

confidence: 91%

“…17,18 This overactivity of the RAS in BPH/2J mice during the active period suggests that there is not an inherent tonic overactivity of the peripheral RAS, but more likely an abnormal regulation of the RAS during the active period. The greater depressor response to enalaprilat is unlikely to merely reflect a greater sensitivity of BPH/2J mice to RAS inhibition because AT 1 receptor inhibition has previously showed no discernable difference in sensitivity of BPN/3J and BPH/2J mice when the AT 1 receptor inhibitor is administered at threshold and maximal doses.…”

Section: Contribution Of Ras To Hypertension In Bph/2j Micementioning

confidence: 98%

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A Novel Interaction Between Sympathetic Overactivity and Aberrant Regulation of Renin by miR-181a in BPH/2J Genetically Hypertensive Mice

et al. 2013

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BPH/2J mice are a genetic model of hypertension developed by Schlager 1 by crossing 8 normotensive strains and selecting for elevated blood pressure (BP). Normotensive BPN/3J control mice were bred concurrently by crossing randomly selected mice from the same base population. Recently, the mechanism of the hypertension has been recognized as neurogenic because ganglion blockade abolished the hypertension in BPH/2J mice.2 Furthermore, spectral analysis of BP revealed greater power in the autonomic frequency band, suggesting overactivity of the sympathetic nervous system (SNS), most prominently during the nocturnal active period.2 BPH/2J mice also display exaggerated daynight differences in BP, which are associated with greater neuronal activity in regions of the hypothalamus and amygdala known to be important for cardiovascular regulation. Given the recent success of renal sympathetic nerve ablation for the treatment of resistant hypertension, 3 the importance of renal influences on the expression of neurogenic hypertension has been highlighted. Importantly, the peripheral renin-angiotensin system (RAS) is closely linked to renal sympathetic nerve activity (RSNA) via its ability to stimulate renin secretion, 4 and also through angiotensin II-mediated facilitation of SNA. 5 However, the interaction of the kidney and renal RAS with SNS-mediated hypertension in BPH/2J mice has not been investigated thoroughly. The role of the RAS has been examined in a variety of ways in BPH/2J mice including by measurement of messenger RNA (mRNA) in tissues and various pharmacological assessments. [6][7][8][9][10] Iwao et al 8 reported normal renin activity in plasma, kidney, and submandibular gland of BPH/2J mice, although others found greater renin activity Abstract-Genetically hypertensive mice (BPH/2J) are hypertensive because of an exaggerated contribution of the sympathetic nervous system to blood pressure. We hypothesize that an additional contribution to elevated blood pressure is via sympathetically mediated activation of the intrarenal renin-angiotensin system. Our aim was to determine the contribution of the reninangiotensin system and sympathetic nervous system to hypertension in BPH/2J mice. BPH/2J and normotensive BPN/3J mice were preimplanted with radiotelemetry devices to measure blood pressure. Depressor responses to ganglion blocker pentolinium (5 mg/kg IP) in mice pretreated with the angiotensin-converting enzyme inhibitor enalaprilat (1.5 mg/kg IP) revealed a 2-fold greater sympathetic contribution to blood pressure in BPH/2J mice during the active and inactive period. However, the depressor response to enalaprilat was 4-fold greater in BPH/2J compared with BPN/3J mice, but only during the active period (P=0.01). This was associated with 1.6-fold higher renal renin messenger RNA (mRNA; P=0.02) and 0.8-fold lower abundance of micro-RNA-181a (P=0.03), identified previously as regulating human renin mRNA. Renin mRNA levels correlated positively with depressor responses to pentolinium (r=0.99; P=0.001), and BPH/2...

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“…Moreover, ACE inhibitors also prevent the breakdown of bradykinin, which releases cerebral vasodilators such as prostacyclin synthetase and nitric oxide (36). Furthermore, it is suggested that BP becomes angiotensin II-dependent during sleep (11,37). It thus can be presumed that perindopril may have an especially marked effect on nighttime BP.…”

Section: Fig 6 Correlation Between δ Pr and The Pr During The Obsermentioning

confidence: 99%

Effect of the Angiotensin-Converting Enzyme Inhibitor Perindopril on 24-Hour Blood Pressure in Patients with Lacunar Infarction: Comparison between Dippers and Non-Dippers

et al. 2005

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The present study assessed the effect of perindopril on the 24-h blood pressure (BP) in hypertensive patients with lacunar infarction using ambulatory BP monitoring (ABPM). There was a 4-week observation period, a 4-week treatment period 1 (perindopril at 2 mg/day), and a 4-week treatment period 2 (perindopril at 4 mg/day). Twenty-seven hypertensive patients with lacunar infarction (10 dippers and 17 non-dippers) were enrolled. The average 24-h BP values were significantly decreased after both treatment periods. When the patients were divided into dippers and non-dippers, perindopril exhibited a different BP-lowering effect in the groups with these two circadian BP patterns. In dippers, daytime BP was significantly decreased, whereas nighttime BP was not, so an excessive fall of nighttime BP was not observed. In non-dippers, both daytime and nighttime BP were decreased, with a stronger BP-lowering effect at night. There was a significant inverse correlation between the magnitude of the change in nighttime BP and the night/day ratio.These results suggested that perindopril could induce a sustained decrease of the 24-h BP in patients with lacunar infarction. In particular, a more pronounced nighttime BP-lowering effect was observed in non-dippers. As the incidence of non-dippers is reported to be high among patients with cerebrovascular disease,

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Twenty-four-hour profiles of plasma renin activity in relation to the sleep-wake cycle

Cited by 99 publications

References 0 publications

Dose Timing of an Angiotensin II Receptor Blocker/Calcium Channel Blocker Combination in Hypertensive Patients With Paroxysmal Atrial Fibrillation

Dose Timing of an Angiotensin II Receptor Blocker/Calcium Channel Blocker Combination in Hypertensive Patients With Paroxysmal Atrial Fibrillation

A Novel Interaction Between Sympathetic Overactivity and Aberrant Regulation of Renin by miR-181a in BPH/2J Genetically Hypertensive Mice

Effect of the Angiotensin-Converting Enzyme Inhibitor Perindopril on 24-Hour Blood Pressure in Patients with Lacunar Infarction: Comparison between Dippers and Non-Dippers

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