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(Hypertension. 2005;45:487.)
© 2005 American Heart Association, Inc.
Editorial Commentaries |
From the Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minn.
Correspondence to Michael J. Joyner, MD, Department of Anesthesiology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905. E-mail joyner.michael@mayo.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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However, when the sympathetic nervous system is destroyed by disease or surgery, blood pressure is highly labile.3 We also know that many "stressors" that evoke a pressor response also evoke marked sympathetic activation, and that the magnitude of these pressor responses can be a harbinger of future hypertension.4,5 Finally, in disease states like congestive heart failure, excessive sympathetic activation is a "bad thing."6,7 If we emphasize these points, sympathetic vasoconstriction seems more important to blood pressure and perhaps survival.
In the middle of this confusion about sympathetic activity and blood pressure lie the baroreflexes that sense changes in arterial pressure and evoke increases in heart rate and sympathetic outflow when blood pressure is "low" and reciprocal responses when blood pressure is "high." Together with their allies in the brain stem and kidney, they make the needed physiological adjustments so that in "normotension" there is an appropriate blood pressure for any given behavioral state.
One mechanism that is
Related Article:
Hypertension 2005 45: 513-521.
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