2010 pa nocturna rew

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2010 pa nocturna rew

  1. 1. ReviewFor reprint orders, please contact reprints@expert-reviews.com The importance of sleep blood pressure Expert Rev. Cardiovasc. Ther. 8(6), 803–809 (2010)Trefor Owen Morgan Blood pressure (BP) varies throughout the day owing to interactions between the sympatheticDepartment of Physiology, University nervous and the renin–angiotensin systems. When awake BP is controlled by sympatheticof Melbourne, Victoria 3010, Australia nervous system activity but during sleep the renin–angiotensin system becomes more important.Tel.: +61 383 445 846 The lower BP during sleep is a more powerful predictor of outcome than the awake BP. CertainFax: +61 383 440 189 individuals do not have the fall in BP with sleep and this worsens the outcome. Inadequatetreforom@unimelb.edu.au handling of sodium by the kidney is an important factor preventing this BP fall. The different drug classes have varying effects on BP during 24 h. Drugs that act independently of the two controlling systems have a similar effect at day and night. Drugs that act on the sympathetic nervous system have a greater effect during the day and little effect during sleep unless the sympathetic system is still active. Drugs that act via the renin–angiotensin system have a greater effect during sleep. Controlling BP during sleep may improve outcome. Keywords : cardiac hypertrophy • dippers • myocardial infarction • nondippers • renin–angiotensin system • sleep blood pressure • stroke • sympathetic nervous system Blood pressure (BP) varies during the 24 h of adjusting to changes in posture and other the day. There are variations owing to acute events, and maintains BP relatively constant. events and an intrinsic variation related to the When an individual sleeps the cardiovascular sleep-awake cycle. A typical pattern is that BP sympathetic nervous system reduces its activ- falls when a person sleeps and stays at a low ity. BP and pulse rate both fall. During sleep, level until they wake [1,2] . BP and pulse rate plasma renin and angiotensin II rise, probably increase on awakening with a further rise in due to the activation of renal baroreceptors [4] . BP on getting out of bed. Typically, BP is at BP is now maintained by the renin–angioten- its highest soon after arising; it then falls with sin system rather than the sympathetic nervous a rise late in the afternoon. It falls again until system. On awakening in the morning, the the individual goes to sleep, when there is a sympathetic nervous system is activated, caus- bigger fall and the cycle repeats. In normo- ing a rise in pulse rate and BP; BP is probably tensive individuals sleep BP is approximately higher at this time due to both systems being 108/63 mmHg, which is 17/15 mmHg lower active. When the person stands there is a fur- than the awake BP [2] . The variation during ther rise in renin secretion as well as a further the day is approximately 10/8 mmHg. The rise in BP to its highest value. With the rise difference between the lowest (during sleep) in BP renin secretion decreases, the morning and highest (awakening and arising) BP is surge is finished and BP returns to the daytime approximately 25/20 mmHg. These are aver- value. If the effect of posture on renin secretion age values and individual people have much is avoided, plasma renin and probably angio- greater variation. The aforementioned is the tensin II is higher when asleep compared with usual pattern but some people do not have a awake [4] . However, in normal living daytime fall when they sleep. The reason for this dif- renin may be higher than the sleep value, as ference is not clear. The daily variation in BP is renin and angiotensin levels vary with altera- predominately owing to altered activity of the tions in posture to control renal blood flow and cardiovascular sympathetic nervous system and glomerular filtration. However, during the day associated alterations in activity of the renin– renin is probably not of great importance in the angiotensin system [3,4] . When awake, the sym- control of BP, as the carotid baroreceptors regu- pathetic nervous system, activated by carotid late this parameter. In a number of countries, baroreceptors, controls BP and the pulse rate, people have a siesta during the day and BP fallswww.expert-reviews.com 10.1586/ERC.10.60 © 2010 Expert Reviews Ltd ISSN 1477-9072 803
  2. 2. Review Morganat this time, and there is a similar rise on awakening [5] . From risk for noncardiovascular mortality [16,17] . In many studiesa study by Brandenberger et al. where the patients slept during night-time BP is the value recorded and reported. It may bethe daytime, there were similar increases in renin secretion as more relevant to report on sleep BP and the time of sleep isoccurred during night-time sleep [4] . best measured with an activgraph. Night-time BP is likely to be less reproducible than sleep BP because the hours of sleep willDippers & nondippers affect the night-time results [18] . Many of the associations thatIf a person has a fall of less than 10 mmHg or 10% of the day- have been made with the night-time BP may be even strongertime BP, they are referred to as nondippers [6] . There is also a with sleep BP.classification of extreme dippers and of reverse dipping whenthe sleep BP is higher than the daytime value. The division Sleep BPinto dippers and nondippers is important because people with A very important study is the Ohasama study [19] , which was aa nondipping pattern have more cardiovascular events and a community study performed in Japan. A total of 1542 patientsworse outcome [6–10] . over 40 years of age (mean age: 61.3 years) were followed for It has been postulated [10] that the reason for nondipping is to 10.6 years. The patients were from the general populationallow the kidney to excrete sodium during sleep [11–13] . During and had an ambulatory BP measurement. The 24-h BP wassleep the kidney tends to conserve both sodium and water, but 122.8/71.8 mmHg, daytime BP was 128.3/75.9 mmHg andif the intake has been high or the kidney has not returned the night-time BP 111.9/63.8 mmHg. BP was also divided into 2-hbody to its correct sodium balance during the awake hours BP intervals based on the time of awakening. The 24-h, daytime andstays elevated to excrete the sodium. In addition to the roles of night-time BP, and the BP at each 2-h interval was compared withthe sympathetic nerves and renin–angiotensin system in con- the incidence of various fatal cardiovascular and cerebrovasculartrolling BP, other factors are also probably involved. This may events. Daytime BP and each 2-h period of daytime BP was asso-be due to an increased circulating plasma volume but it may ciated with an increased incidence of hemorrhagic stroke (Table 1)also be due to a failure of the sympathetic nervous system to but there was no association with ischemic stroke, ischemic heartreduce its activity. disease or other cardiac events. Sleep BP was not associated with There have been relatively few studies of nondipping normo- hemorrhagic stroke but was associated with ischemic cardiac andtensive patients. However, in patients with elevated BP a num- cerebral events, and with other cardiac events. This associationber of observations have been made. Sodium-sensitive patients was not only with the mean BP day and night but with the BP atlose their dipping status when sodium intake is increased [12] . each 2-h interval. BP in the 2-h interval on awakening was notPatients with impaired renal function are frequently nondip- associated with any adverse events.pers [14] , and this is in keeping with an impaired ability to excrete Verdecchia et al. has demonstrated that in poorly controlledsodium. Patients with secondary forms of hypertension (renal hypertensive patients, sleep BP was associated with more car-artery stenosis, hyperaldosteronism) have a higher prevalence diac hypertrophy events [20] . In the Systolic Hypertension inof nondipping. There are also more nondippers among diabetic Europe Trial (SYSEUR), sleep BP prior to entry was a betterpatients with hypertension [15] , and many diabetics have a low- predictor of outcome than either the clinic or daytime BP [21] .renin form of hypertension, an indication of a sodium-loaded Likewise, in the Second Australian National Blood Pressurestate. The reasons for the different dipping status are not fully Study (ANBP2) night-time systolic BP both prior to and duringunderstood and studies are required in which BP, sympathetic treatment was the best predictor of outcome [22,23] . It is not onlynerve activity and renin status are measured throughout 24 h, major cerebro- and cardiovascular events that are associated. Inpreferably with the patient recumbent throughout this time to a study of elderly hypertensive patients, Nagai et al. showedassess the related changes. that sleep systolic BP was more significantly negatively associ- Patients who do not have a fall in BP at night (nondippers) ated with total brain volume than either 24-h or awake BP [24] .have an increased morbidity and mortality from all cardio- Kanemaru et al. showed that high nocturnal systolic BP wasand cerebrovascular causes [6–10] . Such patients have a higher associated with cognitive impairment [25] . These increased asso-24-h BP and cardiac workload, and this may contribute to the ciations of sleep BP with events are present despite the fact thatadverse outcome. An important question is whether it is the sleep BP is lower than daytime BP, indicating that the hormonaltotal 24-h BP and workload that is important or, alternatively, and/or neural activity of the person is important in determiningthe specific BP level during sleep. It is probably the latter [16] , the outcome.and it may be more appropriate to classify this in terms of the The powerful effect of nondipping status on outcome wasachievement of an ideal sleep BP rather than dippers and non- demonstrated in an observational study in diabetic patients [26] .dippers. Night-time BP is a more powerful predictor of outcome In this study, 104 diabetic patients had an ambulatory bloodthan daytime BP and predicts total, cardiovascular and non- pressure monitoring and were classified as risers, reduced dipperscardiovascular mortality even after adjusting for daytime BP. or dippers. There were 16 risers, and 14 individuals died com-Daytime BP predicts all cardiovascular events and strokes, but pared with 40 deaths in the remaining 88 patients. A mortalitywhen adjusted for night-time BP it loses its predictability and rate of 88% was found in the reverse dipping pattern (risers)the only prediction is that low BP is associated with a greater compared with 45% in the remainder. No data are available for804 Expert Rev. Cardiovasc. Ther. 8(6), (2010)
  3. 3. The importance of sleep blood pressure Reviewnight-time BP during the follow-up period, but if the hypothesis Table 1. Hazard ratio for each standard deviationthat sodium status controls dipping is correct, most of these increase in blood pressure.patients would have continued as nondippers as it was unlikelythat a diuretic, which may have altered the dipping status, would Cause of death 24-h BP Awake BP Sleep BPhave been used in these diabetic patients. Total mortality risk 1.76* 1.59* 1.78* There are studies that indicate that it is not be as simple as the Mortality H stroke 2.37* 2.73* 1.42absolute level of sleep BP. Thus, extreme dippers who may havea very low sleep BP have an increased number of adverse cardiac Mortality I stroke 1.60 1.19 1.94*events [27] . Studies indicate that the BP surge may be an important Mortality I cardiac 1.94* 1.58 2.38*predictor of events [28,29] . At the time of awakening when BP rises Mortality NI cardiac 1.51* 1.34 1.70*acutely and reaches its highest level, there are an increased number *p < 0.05.of cerebral and cardiac events [30,31] . However, in the Ohasama BP: Blood pressure; H: Hemorrhagic; I: Ischemic; NI: Nonischemic. Data from [19].study the BP at this time did not predict outcome [19] . This articledoes not address whether sleep BP is more or less important thanBP surges and both probably predict outcome. This may relate associated with increased vascular and cardiac disease [38] .to interactions between the sympathetic and renin–angiotensin Disturbed sleep, such as the sleep apnea syndrome, causes ele-systems at the different times (box 1) . vated BP that is difficult to treat [39] . Depression is associated While this article discusses BP, it is also important to remem- with increased sympathetic activity, decreased and disturbedber that pulse rate falls during sleep, which may also lead to an sleep patterns and increased cardiac mortality [40] . A small studyimprovement in outcome [32] . from Japan indicated that sleep BP was elevated in depressed patients and it is possible that BP elevation at night may beCardiac hypertrophy the precursor causing cardiac hypertrophy as well as increasedA number of human studies indicate that sleep BP is associated morbidity and mortality [41] .with cardiac enlargement [20] . In rats when BP was increased byangiotensin for 6 h during sleep there was cardiac hypertrophy sim- Effect of different drug classes on sleep BPilar to that achieved by increasing the BP over 24 h [33] . However, if A number of drug classes interfere with the sympathetic nervousthe same dose of angiotensin was given during the awake interval, system while others interrupt the renin–angiotensin system.there was no increase in cardiac size. In rats with hypertension As these two systems have different activities over 24 h andinduced using the 2-kidney 1-clip model cardiac hypertrophy was make different contributions to BP, it is likely that drugs thatable to be reversed by reducing BP withcaptopril for 6 h during the sleep periodto a similar extent as achieved with 24-h Box 1. Unresolved conundrum: sleep blood pressure.BP reduction [34] . However, administering • Sleep BP predicts outcome. The lower the betterthe same dose of captopril and reducing • BP surge predicts outcome. The greater the surge the worse the outcome. A large BPBP during the awake hours had no effect surge frequently has a low sleep BPon cardiac size, despite a similar or greater • An acute increase in BP with awakening and standing up normally occurs, but at thisreduction in 24-h BP (Table 2). time there is an increased incidence of cardio- and cerebrovascular events How do we reconcile the above?Renal disease • The lower the sleep BP in people without vascular disease, the betterPatients with renal damage frequently the outcomeexhibit a nondipping status, but there is also • Studies in which the BP surge predicts outcome are usually in older patients whoevidence that in Type 2 diabetes elevated already have vascular disease with stiff blood vesselsnocturnal BP makes it more likely that a • At night during sleep cardiac output is decreased and pulse rate falls. This leads to a low systolic BP and also a low diastolic BP owing to the stiff blood vessels and apatient will develop microalbuminuria. prolonged diastolic timeThus it is important that in diabetic patients, • On awakening, sympathetic activitation increases cardiac output and pulse rate, leadingsleep BP is controlled [35] . If diabetic patients to a greater rise in systolic and diastolic pressure than in people without vascularhave a reversed circadian rhythm (risers), disease, and thus a greater surge. The combination of a higher BP and a more rapidthere is an increased incidence of fatal and pulse rate increases myocardial worknonfatal vascular event occurence [36] . • Coronary arteries in these people have a limited capacity to vasodilate and are not able to deliver the required amount of oxygen, leading to angina, myocardial infarctions,Sleep, depression, sympathetic arrhymias and sudden death. Thus, the cause for the apparent discrepancy may relateactivity & cardiac disease to the presence of stiff arteriesThere are a number of complex interac- • It should be noted that the definition of BP surge varies and is not the same as thetions between these variables [37] . Reduced acute rise in BP seen with awakening and arisingand interrupted hours of sleep have been BP: Blood pressure.www.expert-reviews.com 805
  4. 4. Review Morgan which ARB drugs in doses that have aTable 2. Effect of different time of treatment on 24-h, sleep and full 24-h response have been comparedawake blood pressure, and cardiac hypertrophy. with amlodipine, the fall in BP during Treatment Systolic BP (mmHg) Cardiac index sleep has been greater with the ARB [43] , (mg/g) even though both drugs would have 24‑h Awake Sleep had a plasma level that would produce Control normotensive 117 132 109 2.14 hypertensive rats maximal effect. The probable reason for the greater sleep Control 184 193 171 2.78 BP fall with ACE inhibitors and ARBs is Captopril 75 mg 143 156 124 2.21* that sleep BP is maintained by circulat- Captopril 15 mg 8 AM 172 198 116 2.24* ing levels of angiotensin II. A cross-over Captopril 15 mg 8 PM 169 162 166 2.69 design study comparing perindopril given *p < 0.01 compared with hypertensive control and rats treated during the awake period (8 PM). in the morning or in the evening inferred BP: Blood pressure. that during sleep, a lower level of drug was Data from [34]. needed to obtain the BP fall [44] . Likewise, a study by Smith et al. with trandolopril,act on these systems may have different effects on awake and a very long-acting ACE inhibitor, showed the following over asleep BP. In a randomized, blinded, crossover study Morgan 48-h period [45] . There was a similar fall in day and night-timeet al. compared the effects of different drug classes on day and BP over the first 30 h. The response disappeared 30–40 h afternight-time BP in elderly patients with systolic hypertension who dosing during the day but reappeared 40–48 h after dosinghad not been treated for hypertension [42] . Drugs were used in when the patients slept. During the day carotid baroreceptorsa dose that was known to provide a 24-h or longer duration of predominately control BP, and ACE inhibitors or ARBs requirefull BP response. A dihydropyridine calcium-blocking drug a greater blockade of the renin–angiotensin system to reduce(amlodipine 10 mg) and a thiazide diuretic (hydrochlorthiazide BP. However, at night when circulating angiotensin II controls50 mg) lowered daytime BP slightly more than night-time BP, BP, even a small degree of blockade of angiotensin II formationbut when corrected for the different BPs at these times prior to in plasma will alter BP.medication the falls were similar (Table 3) . A b-blocking drug The importance of different activities of the sympathetic ner-(atenolol 100 mg) lowered daytime BP but had no significant vous system was shown in a study of an a-receptor-blockingeffect on sleep BP. An ACE inhibitor (perindopril 8 mg) low- drug, doxazosin [46] . In patients who were dippers, doxazosinered sleep BP more than daytime BP (Table 3) . Thus, diuretics given at night caused no significant fall in night-time BP, and inand calcium channel-blocking drugs that act independently of fact there was a rise. In nondippers there was a fall of 12 mmHgthe sympathetic nervous and renin–angiotensin systems have a and in risers a fall of 18 mmHg. This indicated that in mostsimilar effect day and night. However, b-blocking drugs had no individuals who are dippers there is an absence of sympatheticeffect on night-time BP because the sympathetic nervous system nervous activity during sleep. However, the persistence of sym-makes little contribution to BP. Conversely, ACE inhibitors pathetic activity during sleep leads to a disturbance of the usualcaused a greater drop in sleep BP than in awake BP. This dif- BP pattern.ference in response would mean that with the same daytime BPcontrol b-blocking drugs convert individuals into nondippers, Importance of time of dosingwhile ACE inhibitors cause individuals to become dippers. This If a drug is used in a dose that provides levels throughout themay explain in part the beneficial effect of ACE inhibitors, 24 h that adequately block the renin–angiotensin system, theparticularly on cardiac hypertrophy. In a number of studies in time of dosing should theoretically not matter. However, many drugs do not have a full 24-h effect. In a study by Hermida Table 3. Effect of different drug classes on day and et al., ramipril 5 mg was given morning or night [47] . The great- night blood pressure. est fall in BP (13.5/11.5 mmHg) occurred in sleep BP with night-time administration. Whether this would translate into Fall in BP (mmHg) different prognostic outcomes is unknown. The Heart Outcome 24‑h Day Night Prevention Evaluation (HOPE) study administered ramipril Diuretics 14.9 15.5 12.5 10 mg at night and had a 22% improvement in a number of CCBDs 14.4 14.8 12.7 events, despite little fall in the clinical (daytime) BP (Table 4) [48] . However, a HOPE substudy indicated a large fall in night-time b-blockers 8.1 11.6 4.4* BP (17/8 mmHg) [49] . In the Perindopril Protection Against ACE inhibitors 11.5 9.5 16.3* Recurrent Stroke Study (PROGRESS) study perindopril 4 mg *p < 0.01 compared with daytime value. given in the morning caused no improvement in the same type ACE: Angiotensin-converting enzyme; BP: Blood pressure; CCBD: Calcium channel-blocking drug. of events [50] . However, in the European Trial on Reduction Data from [42]. of Cardiac Events with Perindopril in Stable Coronary Artery806 Expert Rev. Cardiovasc. Ther. 8(6), (2010)
  5. 5. The importance of sleep blood pressure ReviewDisease (EUROPA) perindopril 8 mg Table 4. Effect of treatment with angiotensin converting enzymegiven in the morning improved outcome inhibitors according to dose and time of administration.similar to the HOPE study [51] . Perindopril4 mg given in the morning may not have Drug used Dose Time Reduction in primary Ref.reduced sleep BP as much as in the other (mg) given end points (%)two studies, and this may explain the Ramipril 10 PM 22 [48]results. When a diuretic was given together Perindopril 4 AM 4 [50]with perindopril there was a greater ben- [50]efit obtained, probably because the diuretic Perindopril + indapamide 4 AM 40increased the fall in BP and increased the Perindopril 8 AM 20 [51]duration of action of perindopril so that itreduced BP during sleep. control of sleep BP and improve prognosis. However, the time An argument can be made that it would be preferable to admin- of administration is of less importance if the drugs are used inister ACE inhibitors and ARBs in the evening. This applies par- a dose that clearly provides 24-h control. Sleep BP should beticularly to the shorter acting drugs, but should be unnecessary measured and it should be normalized.with longer acting drugs given in adequate doses. There wouldappear little reason to administer diuretics and calcium-blocking Expert commentarydrugs in the morning or evening related to their effect on BP, Sleep BP is an important predictor of outcome. A major questionalthough other reasons will influence the choice. b-blocking is whether the absolute level of BP or the variation in BP (dippers,drugs and a-blocking drugs have little effect on sleep BP and nondippers or surge) is more important. The different drug classesthus having a higher concentration during sleep is probably irrel- alter BP differently at various times of the day due to the activitiesevant [37,41] . However, if administered in the evening they would of the control systems. It is important to control BP throughouthave a higher concentration in the morning during the initial 24 h, but control during sleep and on awakening may be moreperiod of increased sympathetic activity. This may reduce the critical than daytime control. This raises the question of whetherearly morning rise in pulse and BP and protect from both overt it may be preferable to give medication in the evening to achieveand silent angina and heart attacks. these aims, and to tailor the drugs used and their time of dosing When comparisons are made between the effect of night-time to achieve the greatest effect.and morning dosing of drugs, it is critical that drugs are used ina dose known to exert its full effect for 24 h. If this is not carried Five-year viewout, spurious conclusions may be drawn. It is also important Sleep BP needs to be controlled. This requires an easy way toto recognize that the pharmacokinetics of drugs may alter the measure BP during sleep and choosing drugs based on theirrates of metabolism during asleep and awake states. Studies action on the controlling systems. It is possible that medicationsare required in which plasma concentrations of the drugs are will be packaged that release their drug components at differentmeasured to determine the fall in BP associated with the same times and rates, allowing effective 24-h BP control.drug concentration. Financial & competing interests disclosureConclusion The author has no relevant affiliations or financial involvement with anyBlood pressure measured during sleep is a more powerful predic- organization or entity with a financial interest in or financial conflict withtor of outcome than when measured at other times of the day. the subject matter or materials discussed in the manuscript. This includesDuring sleep a lower level of BP appears to activate processes employment, consultancies, honoraria, stock ownership or options, expertthat cause vascular disease. ACE inhibitors and ARBs lower testimony, grants or patents received or pending, or royalties.sleep BP preferentially, and this may have significant outcome No writing assistance was utilized in the production of thisbenefits. Administering drugs in the evening may improve the manuscript.Key issues• Sleep blood pressure (BP) predicts cardio- and cerebrovascular events.• Sleep BP is reproducible and is preferred to night-time BP.• Awake BP is controlled by the sympathetic nervous system.• Sleep BP is controlled by the renin–angiotensin system; renin is elevated during sleep.• A lack of a fall in BP during sleep is associated with adverse outcomes.• Failure to excrete sodium during the day due to either excess salt intake or defective renal function leads to an elevated sleep BP.• Drugs that act on the sympathetic nervous system have reduced activity during sleep.• Drugs that act via the renin–angiotensin system have a greater effect during sleep.• Controlling sleep BP has been shown to improve outcome better than controlling daytime BP.www.expert-reviews.com 807
  6. 6. Review MorganReferences from nondipper to dipper in essential ambulatory blood pressure in the SecondPapers of special note have been highlighted as: hypertension. Circulation 96, 1859–1862 Australian National Blood Pressure Study• of interest (1997). (ANBP2). J. Hypertens. 22(Suppl. 1), S58•• of considerable interest 13 Fukuda M, Mizuno M, Yamanaka T et al. (2004).1 Littler WA, Honour AJ, Carter RD, Sleight Patients with renal dysfunction require a 23 Wing LMH, Reid CM, Ryan P, Beilin LJ, P. Sleep and blood pressure. Br. Med. J. longer duration until blood pressure dips Brown MA. Outcome related to on- 3(5979), 346–348 (1975). during the night. Hypertension 52, treatment clinic and ambulatory blood2 Sega R, Corrao G, Bombelli M et al. Blood 1155–1160 (2008). pressure in the Second Australian National pressure variability and organ damage in a 14 Vagaonescu TD, Saadia D, Tuhrim S, Blood Pressure Study (ANBP2). Clin. Exp. general population:results from the Phillips RA, Kaufmann H. Hypertensive Pharmacol. Physiol. 32(7), A7 (2005). PAMELA study (Pressioni Arteriose cardiovascular damage in patients with 24 Nagai M, Hoshide S, Ishikawa J, Shimada Monitorate E Loro Associazioni). primary autonomic failure. Lancet 355, K, Kario K. Ambulatory blood pressure as Hypertension 39, 710–714 (2002). 725–726 (2000). an independent determinant of brain3 Linsell CR, Lightman SL, Mullen PE, 15 Redon J, Plancha E, Swift PA, Pons S, atrophy and cognitive function in elderly Brown MJ, Causon RC. Circadian rhythms Muñoz J, Martinez F. Nocturnal blood hypertension. J. Hypertens. 26, 1636–1641 of epinephrine and norepinephrine in man. pressure and progression to end-stage renal (2008). J. Clin. Endocrinol. Metab. 60, 1210–1215 disease or death in nondiabetic chronic 25 Kanemaru A, Kanemaru K, Kuwajima I. (1985). kidney disease stages 3 and 4. J. Hypertens. The effects of short-term blood pressure4 Brandenberger G, Follenius M, Goichot B, 3, 602–607 (2010). variability and nighttime blood pressure Saini J, Ehrhart J, Simon C. Twenty-four- 16 Boggia J, Li Y, Thijs L et al. Prognostic levels on cognitive function. Hypertens. Res. hour profiles of plasma renin activity in accuracy of day versus night ambulatory 24, 19–24 (2001). relation to the sleep awake cycle. blood pressure: a cohort study. Lancet 370, 26 Astrup AS, Nielsen FS, Rossing P et al. J. Hypertens. 12, 277–283 (1994). 1219–1229 (2007). Predictors of mortality in patients• Important paper indicating how sleep • Good review of the evidence that with Type 2 diabetes with or without night-time blood pressure (BP) is a diabetic nephropathy: a follow-up increases renin secretion. study. J. Hypertens. 25(12), 2479–24855 Stergiou GS, Mastorantonakis SE, Roussias reliable predictor of cardiovascular events. (2007). LG. Intraindividual reproducibility of 17 Dolan E, Stanton A, Thijs L et al. 27 Kario K, Shimada K. Risers and extreme- blood pressure surge upon rising after Superiority of ambulatory over clinic blood dippers of nocturnal blood pressure in nighttime sleep and siesta. Hypertens. Res. pressure measurement in predicting hypertension: antihypertensive strategy for 10, 1859–1864 (2008). mortality: the Dublin outcome study. nocturnal blood pressure. Clin. Exp.6 O’Brien E, Sheridan J, O’Malley K. Dippers Hypertension 46, 156–161 (2005). Hypertens. 26, 177–189 (2004). and non-dippers. Lancet 2, 397 (1998). 18 Eguchi K, Hoshide S, Hoshide Y, Ishikawa 28 Gosse P, Lasserre R, Minifié C, Lemetayer7 White WB. Cardiovascular risk and S, Shimada K, Kario K. Reproducibility of P, Clement J. Blood pressure surge on therapeutic intervention for the early ambulatory blood pressure in treated and rising. J. 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