© 1995 American Heart Association, Inc.
Articles |
Modulation of Cerebral Arteriolar Diameter by Intraluminal Flow and Pressure
From the Department of Neurological Surgery, University of Washington School of Medicine, Seattle.
Abstract We determined whether cerebral arterioles in vitro
adjust their diameters in response to changes in intraluminal flow rate
and pressure. Intracerebral arterioles (38- to 55-µm
diameter) were isolated from Sprague-Dawley rats and
cannulated with a perfusion system that permitted separate control of
intraluminal pressure and flow rates. Increasing pressure at 0 flow, in
20 mm Hg steps from 20 to 100 mm Hg, resulted in myogenic
constriction, which was greatest at 60 mm Hg (
20%). Increasing
flow rate at a constant pressure of 60 mm Hg elicited a biphasic
response. At flow rates of up to 10 µL/min, the arterioles dilated by
up to 14.5±2.2% of their control diameter. At higher (>10 µL/min)
flow rates, however, a progressive restoration of resting diameter was
observed. Application of the nitric oxide synthase
inhibitor
NG-monomethyl-L-arginine
(L-NMMA, 0.1 mmol/L) caused a 15.4±1.7% decrease in control diameter
(at 60 mm Hg, zero flow). Although L-NMMA did not affect the responses
to increases in pressure or to vasodilators (adenosine and pH
6.8 buffer), it abolished the dilator responses to flow rate increases
and to acetylcholine. In contrast, inhibition of
prostaglandin synthesis by indomethacin (10
µmol/L) had no effect on flow-induced dilation. These results
show that changes in intraluminal flow rates and pressure can
independently influence cerebral arteriolar tone and suggest that the
flow-induced dilator responses of cerebral arterioles are mediated
by an arginine metabolite, such as nitric oxide.
Key Words: shear stress • flow velocity • cerebral circulation • nitric oxide • myogenic response
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