Masked and white coat hypertension, the double trouble of large arteries: A systematic review and meta‐analysis

Antza, Christina; Vazakidis, Polychronis; Doundoulakis, Ioannis; Bouras, Emmanouil; Haidich, Anna‐Bettina; Stabouli, Stella; Kotsis, Vasilios

doi:10.1111/jch.13876

Cited by 20 publications

(15 citation statements)

References 26 publications

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“…Based on previous [26,27] and current observations, we conclude that chronic foot shock stress induces elevated AQP1 expression in the kidneys via the renal sympathetic nerve system, renin-angiotensin system, and oxidative stress by regulation of vasopressin level. These findings have been schematized in Figure 6.…”

Section: Discussionsupporting

confidence: 70%

Role of Renin-Angiotensin System, Renal Nerve System, and Oxidative Stress in Chronic Stress-Induced Renal Expression of Aquaporin-1 in Rats

X¹,

Y²,

Wang³

et al. 2021

austinjnephrolhypertens

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Aims: To investigate the renal aquaporin-1 (AQP1) expression under chronic stress (induced by foot shock) condition and possible mechanisms involved in rats. Methods: The chronic stress model was established in male Sprague Dawley (SD) rats by foot shock for two weeks. Rats were randomly divided into control group, chronic stress group, renal denervation group, renal denervation plus chronic stress group, captopril (an angiotensin I converting enzyme inhibitor, ACEI) plus chronic stress group and tempol (a superoxide dismutase mimetic) plus chronic stress group. Body weight, food intake, water intake, blood pressure and heart rate were monitored. Real-time PCR was used to detect the mRNA level of AQP1 in the renal tissue. Immunohistochemistry stain was used to observe the expression and location of AQP1 in rat kidneys. Results: Chronic stress reduced body weight gain and food intake, while it significantly increased systolic blood pressure and renal expressions of mRNA and protein of AQP1 (P<0.05) as compared with control group. Renal denervation and tempol treatments did not affect stress-induced decreases of body weight gain and food intake. Renal denervation, captopril and tempol treatments decreased systolic blood pressure. Compared with the chronic stress group, mRNA and protein expression of AQP1 was decreased (P<0.05) in renal denervation plus chronic stress group, captopril plus chronic stress group and tempol plus chronic stress group. Conclusion: Chronic stress induces increase of the AQP1 expression in kidney, which is regulated by renal nerve system, renin-angiotensin system and oxidative stress.

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Section: Discussionsupporting

confidence: 70%

Role of Renin-Angiotensin System, Renal Nerve System, and Oxidative Stress in Chronic Stress-Induced Renal Expression of Aquaporin-1 in Rats

X¹,

Y²,

Wang³

et al. 2021

austinjnephrolhypertens

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“…A meta‐analysis in this issue of the Journal of Clinical Hypertension adds to the current knowledge by evaluating pulse wave velocity (PWV), an index of arterial stiffness, in WCH and MH in comparison with normotension and sustained hypertension 7 . Seven studies including 2352 subjects were assessed.…”

Section: Introductionmentioning

confidence: 99%

Pulse wave velocity in white coat and masked hypertension

Pierdomenico

Coccina

Madonna

2020

J of Clinical Hypertension

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| INTRODUC TI ONOut-of-office blood pressure (BP) measurement has given the opportunity to detect various hypertension phenotypes. Among them, white coat hypertension (WCH), ie, high clinic and normal out-of-office BP and masked hypertension (MH), that is, normal clinic and high out-of-office BP have been extensively studied in the past years.Their prognostic relevance 1-3 and target organ involvement, 4-6 which is frequently an intermediate stage toward cardiovascular events, have been assessed. Concerning the prognostic impact, it appears still debated in WCH, 1,2 whereas there seems to be unanimous consensus about the adverse prognostic value of MH. 1,3 In the same way, cardiac and vascular involvement look controversial in WCH,4,5 while there is substantial evidence of target organ damage in MH. 6 A meta-analysis in this issue of the Journal of Clinical Hypertension adds to the current knowledge by evaluating pulse wave velocity (PWV), an index of arterial stiffness, in WCH and MH in comparison with normotension and sustained hypertension. 7 Seven studies including 2352 subjects were assessed. Subjects with MH and WCH had significantly higher PWV than normotensive ones (d = 0.96 m/s, 95% CI: 0.49-1.42 for MH and d = 0.85 m/s, 95% CI: 0.48-1.22 for WCH). Moreover, subjects with MH and WCH had lower PWV than sustained hypertensive ones (d = −0.70 m/s, 95% CI: −0.87 to −0.54 for MH and d = −0.75 m/s, 95% CI: −1.52 to 0.02 for WCH). No significant difference between MH and WCH was observed (d = 0.06 m/s, 95% CI −1.04 to 1.15). Thus, the authors concluded that WCH and MH are not clinically innocent. Looking at BP values of selected studies, in comparison with normotensive subjects, clinic BP and 24-hour BP were higher, respectively, by 23/11 mm Hg and 4/2 mm Hg in subjects with WCH and, respectively, by 8/2 mm Hg and 16/10 mm Hg in those with MH. Measurement of PWV is a simple and noninvasive way to assess arterial stiffness, a manifestation of vascular damage associated with hypertension and aging. 8 Various studies have shown that arterial stiffness independently predicts cardiovascular events and it is now accepted as an intermediate end point. 8 The mechanisms underlying arterial stiffening are not yet completely clear. In the context of long-standing hypertension, it has been suggested that endothelial damage, smooth muscle tone, inflammation, oxidative stress, renin-angiotensin system activity, and extracellular matrix turnover and integrity might be involved in this process. 8 However, beyond the impact of vascular structural changes on PWV, this parameter may also by influenced by intercurrent BP modifications. 9Indeed, a powerful confounder of PWV interpretation may be BP.Increased BP augments the arterial wall tension and adds functional arterial stiffness, that is, vessels become stiffer at higher pressures. 9Therefore, the effect of BP increase should be taken into account during PWV analysis. Subjects with WCH have substantial clinic BP increase, at variance with those with normotension or MH, while m...

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“…However, their prognostic significance has to be demonstrated beyond the established risk factors such as blood pressure (BP), cholesterol levels, diabetes mellitus, smoking, as well as age and sex 3 . It has been shown that increased arterial stiffness may predict cardiovascular events in asymptomatic individuals with 4 or without overt CV disease 5 . As such, arterial stiffness has been recommended as a useful prognostic biomarker 6 .…”

Section: The Application Of Arterial Stiffness Measurements In Clinicmentioning

confidence: 99%

Measuring arterial stiffness in clinical practice: Moving one step forward

Cheng¹,

Chen

2020

J of Clinical Hypertension

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Arterial stiffness or arteriosclerosis is the degeneration of the arterial beds, which may be the earliest detectable manifestations of adverse functional and structural changes in the arterial wall. 1 It should be differentiated from atherosclerosis, defined as an occlusive arterial disease characterized by lipid oxidation, inflammation, and plaque formation in the arterial wall. 2 With cumulating evidence, arterial stiffness has been established as an important parameter for the assessment of cardiovascular (CV) risk.

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Masked and white coat hypertension, the double trouble of large arteries: A systematic review and meta‐analysis

Cited by 20 publications

References 26 publications

Role of Renin-Angiotensin System, Renal Nerve System, and Oxidative Stress in Chronic Stress-Induced Renal Expression of Aquaporin-1 in Rats

Role of Renin-Angiotensin System, Renal Nerve System, and Oxidative Stress in Chronic Stress-Induced Renal Expression of Aquaporin-1 in Rats

Pulse wave velocity in white coat and masked hypertension

Measuring arterial stiffness in clinical practice: Moving one step forward

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