Prevention or attenuation of baroreceptor resetting by pulsatility during elevated pressure.
Acute static elevation of arterial pressure increases the pressure threshold for activation of baroreceptors (acute resetting). The purpose of this study was to test the hypothesis that pulsatility during acute elevation of pressure modifies this acute resetting. Activity was recorded in 21 single baroreceptor units from the isolated carotid sinuses of dogs anesthetized with chloralose. Single-unit pressure thresholds were determined with a slow ramp increase in pressure. After a control period of static pressure at 25 to 50 mm Hg, the pressure threshold averaged 69 +/- 4 (SE) mm Hg. Three graded levels of static pressure were held for 5 to 15 minutes. The levels averaged 76 +/- 4, 115 +/- 6, and 170 +/- 5 mm Hg. The corresponding nerve activity during these periods was 0, 44 +/- 6, and 63 +/- 6 spikes per second, and the resulting increases in pressure threshold averaged 10 +/- 1, 17 +/- 2, and 26 +/- 3 mm Hg, respectively. In contrast, during equivalent elevations of pulsatile pressure, nerve activity averaged 20 +/- 3, 37 +/- 4, and 61 +/- 5 spikes per second, and the increases in pressure threshold averaged 0 +/- 4, 14 +/- 2, and 24 +/- 2 mm Hg, respectively. In some units, the pressure threshold decreased following elevation of pulsatile pressure. The results indicate that: pulsatility during elevation in pressure prevents or attenuates the acute baroreceptor resetting except at maximal pressure; upward resetting occurs with elevation of static pressure even when there is no nerve activity during the period of elevated pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
- Copyright © 1987 by American Heart Association