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AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 5 1241-R1249, Copyright © 1994 by American Physiological Society
ARTICLES |
D. C. Randall, D. R. Brown, L. V. Brown and J. M. Kilgore
Department of Physiology and Biophysics, University of Kentucky College of Medicine, Lexington 40536-0084.
The object of this experiment is to analyze the neural control of arterial blood pressure (BP) during rest and a sudden behavioral stress. Sprague-Dawley rats were classically conditioned by following a 15-s tone (CS+) with a 0.5-s tail shock. Bipolar renal nerve electrodes and a caudal artery catheter were implanted. Two days later BP and sympathetic nervous activity (SNA) were recorded in the behaviorally trained animals. The CS+ evoked a large initial increase in BP (peak, 14 +/- 5 mmHg, mean +/- SD; n = 12) that lasted 3.9 +/- 0.8 s. An abrupt (latency = 0.16 +/- 0.03 s), short (duration = 0.58 +/- 0.12 s), and intense (4.09 +/- 1.02 times average control) burst in sympathetic activity preceded this first component (C1) of the BP conditional response. The size of C1 was related to the magnitude of the SNA burst. SNA then fell below control; this quiet period preceded a fall in BP after the C1 peak. Pressure rose again (C2; peak = 6 +/- 3 mmHg, average increase = 3 +/- 3 mmHg) for the remainder of the CS+. SNA increased to 1.24 +/- 0.14 of control during this second component of the BP conditional response. Ganglionic blockade eliminated the BP and SNA conditional response (n = 3). The C1 pressure increase appears to result from an "open-loop" process in which a brief barrage of nerve activity governs BP changes lasting several seconds. The quite period probably results from a negative feedback (i.e., baroreflex) relationship between SNA and BP.(ABSTRACT TRUNCATED AT 250 WORDS)
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