Salt supresses baseline muscle sympathetic nerve activity in salt-sensitive and salt-resistant hypertensives

The objective of our study was to evaluate the role of the baroreflex control of peripheral sympathetic nervous system on the increase of muscle sympathetic nerve activity (MSNA) in salt-sensitive (SS) and salt-resistant (SR) hypertensives under low salt diet. In phase I mild-to-moderate hypertensiv...

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Bibliographic Details
Published in:Journal of human hypertension Vol. 16; no. 12; pp. 843 - 850
Main Authors: Abrahão, S B, Tinucci, T, Santello, J L, Mion, Jr, D
Format: Journal Article
Language:English
Published: England Nature Publishing Group 01-12-2002
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Summary:The objective of our study was to evaluate the role of the baroreflex control of peripheral sympathetic nervous system on the increase of muscle sympathetic nerve activity (MSNA) in salt-sensitive (SS) and salt-resistant (SR) hypertensives under low salt diet. In phase I mild-to-moderate hypertensive patients (n=5) received three diet periods: a first regular salt (RS1), a low salt (LS=20 meq Na+/day), followed by a second regular salt diet (RS2) with a 7-day duration of each. At the end of each period, sympathetic and heart rate baroreflex control were recorded. Baseline MSNA varied (P<0.005) from 18+/-8 (RS1) to 32+/-9 (LS) and to 14+/-9 (RS2) bursts per minute (bpm). In phase II additional patients (n=6) were included to have baseline MSNA, sympathetic and heart rate baroreflex control evaluated at the end of the LS and RS2. For all patients (n=11), there was a significant decrease of MSNA from 36+/-4 to 20+/-8 bpm on day 7 of LS to RS2 (P<0.05). The response of MSNA to a salt restriction was similar for SS and SR patients, who showed a change from 32+/-6 to 18+/-11 and from 36+/-9 to 17+/-7 bpm for SS and SR on day 7 of LS and RS2 diets, respectively (P<0.05). MSNA baroreflex gain was similar during phenylephrine infusions at day 7 of LS and RS2 (5.1+/-1.6 and 6.1+/-2.9 bpm/mmHg), but it was reduced under LS during sodium nitroprusside infusion (19.5+/-4.9 vs 8.9+/-0.7 bpm/mmHg) (P<0.05) for the whole group. Baroreflex control of MSNA was also similar during phenylephrine infusions under LS and RS2 diets for SS (4.0+/-0.9 and 3.3+/-0.2 bpm/mmHg) and for SR patients (10.1+/-2.5 and 5.6+/-1.5 bpm/mmHg). During nitroprusside infusion, baroreflex gain was significantly greater under RS2 for SR patients (19.5+/-2.6 bpm/mmHg) when compared to LS (11.2+/-5.2 bpm/mmHg) and the same significant difference was observed among SS patients (14.4+/-4.7 and 9.1+/-3.6 bpm/mmHg under RS2 and LS diets, respectively). There was no difference in heart rate baroreflex gain between LS and RS2 diets. Data support the hypotheses that (1) sodium supresses baseline MSNA in SS and SR hypertensives and (2) sodium restriction may impair baroreflex control of MSNA in SR and SS mild-to-moderate hypertensive patients during blood pressure reductions.
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ISSN:0950-9240
1476-5527
DOI:10.1038/sj.jhh.1001492