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Sympathetic control of BP and BP variability in borderline hypertensive rats on high- vs. low-salt diet.

作者信息

Brown D R, Li S G, Lawler J E, Randall D C

机构信息

Center for Biomedical Engineering, University of Kentucky, Lexington, Kentucky 40536, USA.

出版信息

Am J Physiol. 1999 Sep;277(3):R650-7. doi: 10.1152/ajpregu.1999.277.3.R650.

Abstract

This experiment tested the effect of a high-salt diet on the interaction between arterial blood pressure (BP) and sympathetic nerve activity (SNA) at rest and during a controlled behavioral stress at an early stage in the development of hypertension in borderline hypertensive rats (BHR). Ten rats were maintained on a high-salt diet (8% NaCl) while 14 were fed a low-salt diet (0.8% NaCl) for 8 wk. They were trained in a Pavlovian paradigm by following a conditional stimulus tone (CS+) with a 0.5-s shock. SNA and BP were measured by implanted electrodes around the left renal nerve and a catheter in the femoral artery, respectively. There were no detectable between-group differences in BP or in BP variability in the resting animal at the end of the 8-wk dietary treatment. Moreover, there were no significant between-group differences in the changes in SNA evoked by the CS+ tone. Conversely, the amplitude of the initial conditional increase in BP was significantly (P < 0.05) larger in the high-salt (6 +/- 0.6 mmHg; mean +/- SEM) compared with the low-salt (4 +/- 0.4 mmHg) group. In addition, the BP excursion (peak/trough) during CS+ was larger in the high (18.2 +/- 6.1 mmHg)- vs. low-salt (5.8 +/- 0.4 mmHg) diet-fed subjects. The ratio of the average percent change in mean BP to the average percent change in SNA at the beginning of CS+ was 0.029 +/- 0.004 for the low-salt group and 0.041 +/- 0.006 for the high-salt group. We find that, before the development of overt hypertension, the enhanced conditional BP response in the high-salt BHR appears to reside at the interface between changes in SNA and the effector response and not within the central nervous system. These observations help explain the increasing BP variability typically observed with the development of hypertension in humans.

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