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AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 3 666-R673, Copyright © 1989 by American Physiological Society
ARTICLES |
J. W. Osborn, R. F. Taylor and L. P. Schramm
Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
The present study was conducted to determine whether sympathetic vasoconstrictor activity is a determinant of mean arterial pressure (MAP) hours and days after cervical spinal transection (CST) in unanesthetized rats. MAP on the 2 days before CST was 107.2 +/- 3.6 and 103.3 +/- 3.0 mmHg, respectively, and fell to 77.7 +/- 1.1 mmHg on day 1 after CST. MAP returned to control levels over the course of the study and, by day 9 after CST, was not statistically different from control (98.6 +/- 3.4 mmHg). Neither autonomic ganglionic blockade nor alpha-adrenergic blockade affected MAP the 1st day after CST. Similarly, alpha-adrenergic blockade was without effect on days 3, 5, and 7 after CST. Administration of a vasopressin V1-antagonist had no effect on MAP on day 1 or day 8 after CST. However, blockade of angiotensin-converting enzyme with captopril decreased arterial pressure both on day 1 (-22.1 +/- 2.6 mmHg) and day 8 (-23.3 +/- 2.9 mmHg) after CST. We conclude that neither sympathetic nor vasopressin vasoconstrictor activity affected MAP within the 1st wk after CST. Although the vasoconstrictor actions of angiotensin II were important, these effects were not responsible for the normalization of MAP observed after CST.
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