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(Circulation. 2005;112:786-788.)
© 2005 American Heart Association, Inc.

Editorial

Sleep and Hypertension

A Challenge for the Autonomic Regulation of the Cardiovascular System

Jacopo M. Legramante, MD; Alberto Galante, MD

From the Dipartimento di Medicina Interna, Università di Roma "Tor Vergata," and IRCCS S. Raffaele, Tosinvest Sanità, Rome, Italy.

Correspondence to Jacopo M. Legramante, MD, Dipartimento di Medicina Interna, Università di Roma "Tor Vergata," Via O. Raimondo, 8, 00173 Roma, Italy. E-mail legramante@med.uniroma2.it

Key Words: Editorials • baroreceptors • hypertension • nervous system, autonomic • sleep

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Even though sleep is widely considered to be a restorative and refreshing process, it is characterized by complex activity of the cardiovascular autonomic mechanisms and by relevant changes of arterial pressure and heart rate. It has been widely reported that fluctuations and variability of cortical and visceral activities involve a differential autonomic regulation of the cardiovascular system in relationship to different sleep cycles. During non–rapid eye movement (REM) sleep, arterial pressure and heart rate tend to decrease, whereas periods of relative hypertension and tachycardia characterize REM periods. With regard to the cardiovascular autonomic modulation, non-REM sleep is characterized by a vagal predominance, whereas during REM sleep, a relative increase in sympathetic activity is demonstrated by an increased sympathetic outflow to muscle blood vessels.^1–3

See p 849

Therefore, this continuous cycling of non-REM and REM phases, with the consequent cardiovascular autonomic changes, makes sleep a period of considerable physiological turbulence characterized by sudden and abrupt blood pressure and heart rate changes. This cardiovascular instability has stimulated the investigation of the neural mechanisms involved in maintaining the cardiovascular homeostasis during the different sleep phases. The first pivotal study conducted with the Oxford technique in normotensive and hypertensive subjects⁴ clearly showed that changes in baroreflex function investigated by quantifying the reflex RR interval lengthening in response to a pharmacologically induced increase in systolic blood pressure (obtained through intravenous injection of phenylephrine), occurred ongoing from wakefulness to sleep. These changes consisted of an increase in the reflex sensitivity and of a resetting, moving the . . . [Full Text of this Article]

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