The Primary Benefits of Angiotensin-Converting Enzyme Inhibition on Cardiac Remodeling Occur During Sleep Time in Murine Pressure Overload Hypertrophy

Martino, Tami A.; Tata, Nazneen; Simpson, Jeremy A.; Vanderlaan, Rachel D.; Dawood, Fayez; Kabir, M. Golam; Khaper, Neelam; Cifelli, Carlo; Podobed, Peter; Liu, Peter P.; Husain, Mansoor; Heximer, Scott P.; Backx, Peter H.; Sole, Michael J.

doi:10.1016/j.jacc.2010.11.022

Cited by 81 publications

(53 citation statements)

References 30 publications

(31 reference statements)

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“…In 1 recent human study a 5 mm Hg reduction in sleep-time systolic BP caused a 17% reduction in adverse cardiovascular events in a hypertensive population, 96 and, in hypertensive mice, captopril prevented cardiovascular remodeling only when administered before sleep. 97 …”

Section: Hypertensionmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

Kasai

Floras²,

Bradley³

2012

Circulation

330

207

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Sleep apnea occurs in Ϸ5% to 10% of the general population, regardless of race and ethnicity. 1 By contrast, in patients with cardiovascular diseases (CVDs), its prevalence, depending on the specific disorder surveyed, can range between 47% and 83%. [2][3][4] One form, central sleep apnea (CSA), is rare in the general population, but is detected often in conditions characterized by sodium and water retention, such as heart failure (HF). 2 Such epidemiological observations raise several important and as yet unresolved questions: What accounts for this remarkable concentration of sleep apnea among patients with CVD and its association with fluid retaining states? Does obstructive sleep apnea (OSA) predispose at-risk individuals to develop, over time, hypertension, coronary artery disease, stroke, or HF? Conversely, could mechanisms engaged by CVD, such as activation of the sympathetic nervous and renin-angiotensin-aldosterone systems, with consequences including renal sodium retention, contribute over time to the development or exacerbation of sleep apnea? From the clinical perspective, is sleep apnea, when present in patients with CVD an epiphenomenon, perhaps related to ageing, or a causal contributor to worse prognosis? And if so, are there now sufficient data to recommend randomized controlled trials to determine whether specific treatment of sleep apnea can reduce mortality or cardiovascular event rates? Our objectives, in this review, are to provide novel insight into each of these specific questions by integrating into our contemporary understanding of relationships between sleep apnea and CVD 5 newer epidemiological, observational, mechanistic, and trial data; to introduce a hypothetical model of bidirectional causality; and to consider directions for future research. Normal SleepIn healthy subjects, during non-rapid eye movement sleep (which constitutes Ϸ85% of total sleep time), efferent sympathetic nerve activity (SNA) diminishes and vagal tone increases, resulting in reductions in metabolic rate, blood pressure (BP), and heart rate (HR). 6,7 Thus, although sleep is, in general, a stable state of cardiovascular quiescence, this tableau can be interrupted both normally, by the intermittent surges in SNA, BP, and HR characteristic of rapid eye movement sleep (but comprising only 15% of total sleep time), 6 and pathologically, whether because of fitful sleep or shorter overall sleep time, as evident in patients with HF or drug-resistant hypertension, 8,9 or by coexisting sleep apnea, whether obstructive (OSA) or central (CSA).

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Section: Hypertensionmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

Kasai

Floras²,

Bradley³

2012

Circulation

330

207

View full text Add to dashboard Cite

show abstract

“…Indeed, several clinical studies have discovered that nighttime angiotensinconverting enzyme inhibitor achieves better BP control and is associated with lower risk for total cardiovascular disease events (15)(16)(17)(18). Furthermore, study in mice showed that rest-time angiotensin-converting enzyme inhibitor results in improved cardiac remodeling even when controlled for BP (19). Additional therapy aimed at facilitating the resynchronization using both behavioral (e.g., feeding, exercise, lighting conditions) and pharmacological modifications (melatonin) may be effective.…”

Section: Inflammationmentioning

confidence: 99%

Beating against the clock

Zhang

Jain

2016

Proc. Natl. Acad. Sci. U.S.A.

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“…In this model, a 10-h/10-h light-dark cycle was used to disrupt the circadian clock in mice, which led to increased cardiac hypertrophy and reduced contractility compared with mice on a normal 12-h/ 12-h light-dark cycle (86). Furthermore, in this same model, it was shown that nonblood pressure-dependent antihypertrophic benefits of the angiotensin-converting enzyme (ACE) inhibitor captopril were increased more during the inactive phase than the active phase (87). Interestingly, using the same model, it was demonstrated that multiple genes involved in cardiac remodeling, glycolysis, and fatty acid metabolism were significantly altered.…”

Section: Cardiovascular System and The Kidneymentioning

confidence: 99%

Mechanism of the circadian clock in physiology

Richards

Gumz

2013

American Journal of Physiology-Regulatory, Integrative and Comp

119

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It has been well established that the circadian clock plays a crucial role in the regulation of almost every physiological process. It also plays a critical role in pathophysiological states including those of obesity and diabetes. Recent evidence has highlighted the potential for targeting the circadian clock as a potential drug target. New studies have also demonstrated the existence of "clock-independent effects" of the circadian proteins, leading to exciting new avenues of research in the circadian clock field in physiology. The goal of this review is to provide an introduction to and overview of the circadian clock in physiology, including mechanisms, targets, and role in disease states. The role of the circadian clocks in the regulation of the cardiovascular system, renal function, metabolism, the endocrine system, immune, and reproductive systems will be discussed.

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The Primary Benefits of Angiotensin-Converting Enzyme Inhibition on Cardiac Remodeling Occur During Sleep Time in Murine Pressure Overload Hypertrophy

Cited by 81 publications

References 30 publications

Sleep Apnea and Cardiovascular Disease

Sleep Apnea and Cardiovascular Disease

Beating against the clock

Mechanism of the circadian clock in physiology

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