Published Online
on May 1, 2008

A more recent version of this article appeared on July 1, 2008

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Submitted on November 13, 2007
Revised on November 27, 2007
Accepted on December 5, 2007

Autonomic Neural Control of the Cerebral Vasculature. Acute Hypotension

Shigehiko Ogoh PhD^*; R. Matthew Brothers PhD; Wendy L. Eubank MS; and Peter B. Raven PhD

From the Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, Fort Worth, Texas.

^* To whom correspondence should be addressed. E-mail: sogoh{at}hsc.unt.edu.

Background and Purpose—The effect of antihypertensive drugs on autonomic neural control of the cerebral circulation remains unclear. This study was designed to compare middle cerebral artery mean blood velocity responses to acute hypotension with and without ₁-adrenoreceptor blockade (Prazosin) in young, healthy humans.

Methods—Acute hypotension was induced nonpharmacologically in 6 healthy subjects (mean±SE; 28±2 years) by releasing bilateral thigh cuffs after 9 minutes of suprasystolic resting ischemia before and after an oral dose of Prazosin (1 mg/20 kg body weight).

Results—Prazosin had no effect on thigh cuff release-induced reductions in mean arterial pressure and middle cerebral artery mean blood velocity. However, Prazosin attenuated the amount of peripheral vasoconstriction through the arterial baroreflex as evidenced by a slower return of mean arterial pressure to baseline (P=0.03). Immediately after cuff release, cerebral vascular conductance index increased through cerebral autoregulation and returned to resting values as a result of an increased perfusion pressure mediated through arterial baroreflex mechanisms. The rate of regulation, an index of cerebral autoregulation, was attenuated with Prazosin (control versus Prazosin; rate of regulation=0.204±0.020 versus 0.006±0.053/s, P=0.037). In addition, as mean arterial pressure was returning to resting values, the rate of change in cerebral vascular conductance index was decreased with Prazosin (0.005±0.006/s) compared with control (0.025±0.005/s; P=0.010).

Conclusions—These data suggest that during recovery from acute hypotension, decreases in cerebral vascular conductance index were mediated by increases in arterial blood pressure and sympathetically mediated cerebral vasoconstriction.

Key words: arterial blood pressure • middle cerebral artery blood velocity • sympathetic activity

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