Sleep and vascular disorders

被引:21
作者
Plante, Gerard E. [1 ]
机构
[1] Univ Sherbrooke, Inst Pharmacol, Dept Med Nephrol, Sherbrooke, PQ J1H 5N4, Canada
[2] Univ Sherbrooke, Dept Physiol, Sherbrooke, PQ J1H 5N4, Canada
[3] Univ Sherbrooke, Dept Pharmacol, Sherbrooke, PQ J1H 5N4, Canada
[4] Univ Sherbrooke, Inst Geriatr, Sherbrooke, PQ J1H 5N4, Canada
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2006年 / 55卷 / 10期
关键词
D O I
10.1016/j.metabol.2006.07.013
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It is not surprising that cardiovascular diseases such as congestive heart failure and coronary insufficiency can give rise to varying degrees of sleep impairment; it is less readily appreciated that certain physiologic events occurring during sleep-as well as long-term unsatisfactory sleep-may cause or increase the risk of cardiovascular conditions such as hypertension, atherosclerosis, stroke, and cardiac arrythmias. Heart rate abnormalities during sleep in normotensive subjects predict later cardiovascular disease, and their early identification alerts the physician to undertake preventive measures. Maneuvers, such as induction of hypoxia, can elicit abnormal blood pressure responses during sleep, and such responses have been used to identify impending cardiovascular problems that could become therapeutic targets. The spontaneously hypertensive rat has been used to examine the effect of sympathetic nervous system (SNS) activity on the heart under a variety of experimental conditions, including quiet and paradoxical sleep. The results have disclosed significant differences between the responses of spontaneously hypertensive rats and normal rats to SNS stimulation. Exploration of other pathophysiologic pathways affected by exposure to light and dark, including those responsive to the cyclic production of melatonin, will improve our understanding of the effect of disruptions of the circadian cycle on cardiovascular function. There is growing evidence that melatonin can influence important processes such as fluid, nitrogen, and acid-base balance. Human subjects whose nocturnal arterial blood pressure fails to show the "normal" decrement during sleep ("nondippers") are also prone to sleep poorly, exhibit increased SNS activity during sleep, and have an increased risk of total and cardiovascular disease mortality. Chronic sleep deficit is now known to be a risk factor for obesity and may contribute to the visceral form of obesity that underlies the metabolic syndrome. The rising prevalence of obstructive sleep apnea and central sleep apnea is linked to the modem-day epidemic of obesity. Obstructive sleep apnea is associated with an enhanced risk of having a new stroke or a transient ischemic attack. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:S45 / S49
页数:5
相关论文
共 36 条
[1]   Daytime blood pressure elevation after nocturnal hypoxia [J].
Arabi, Y ;
Morgan, BJ ;
Goodman, B ;
Puleo, DS ;
Xie, AL ;
Skatrud, JB .
JOURNAL OF APPLIED PHYSIOLOGY, 1999, 87 (02) :689-698
[2]   BORDERLINE HYPERTENSION - A 24-HOUR ABNORMALITY [J].
BERGBRANT, A ;
HANSSON, L ;
JERN, S .
AMERICAN JOURNAL OF HYPERTENSION, 1993, 6 (08) :713-718
[3]   Epidemiology, trends, and morbidities of obesity and the metabolic syndrome [J].
Bray, GA ;
Bellanger, T .
ENDOCRINE, 2006, 29 (01) :109-117
[4]   Obstructive sleep apnea as a cause of systemic hypertension - Evidence from a canine model [J].
Brooks, D ;
Horner, RL ;
Kozar, LF ;
RenderTeixeira, CL ;
Phillipson, EA .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (01) :106-109
[5]   The metabolic syndrome: prevalence in worldwide populations [J].
Cameron, AJ ;
Shaw, JE ;
Zimmet, PZ .
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA, 2004, 33 (02) :351-+
[6]   Melatonin-induced modulation of glucose metabolism in primary cultures of rabbit kidney-cortex tubules [J].
Derlacz, RA ;
Poplawski, P ;
Napierala, M ;
Jagielski, AK ;
Bryla, J .
JOURNAL OF PINEAL RESEARCH, 2005, 38 (03) :164-169
[7]   EFFECT OF INDUCING NOCTURNAL SERUM MELATONIN CONCENTRATIONS IN DAYTIME ON SLEEP, MOOD, BODY-TEMPERATURE, AND PERFORMANCE [J].
DOLLINS, AB ;
ZHDANOVA, IV ;
WURTMAN, RJ ;
LYNCH, HJ ;
DENG, MH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (05) :1824-1828
[8]  
Frisina N., 1998, Blood Pressure, V7, P76
[9]   Metabolic syndrome: Connecting and reconciling cardiovascular and diabetes worlds [J].
Grundy, SM .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2006, 47 (06) :1093-1100
[10]  
HATTORI A, 1995, BIOCHEM MOL BIOL INT, V35, P627