Sodium depresses arterial baroreceptor reflex function in normotensive humans.

Journal Article (Clinical Trial;Journal Article)

Sodium may contribute to the pathogenesis of hypertension by impairing arterial baroreceptor reflex function. The objectives of this study were to 1) determine whether a high sodium diet depresses arterial baroreceptor reflex function in normotensive humans, and 2) determine whether alterations in baroreceptor reflex function are related to changes in arterial compliance. Seventeen normotensive men, aged 30 +/- 2 years, received 10 and 200 meq sodium per day diets, each for 5 days, in a randomized crossover trial. Carotid baroreceptor reflex function was assessed by measuring the blood pressure response to sequential neck suction (0, -10, -20, and -30 mm Hg) and neck pressure (0, +10, +20, and +30 mm Hg). Forearm vascular resistance was determined by venous occlusion plethysmography. Arterial compliance was evaluated by calculating the quotient of the diastolic blood pressure decay time constant and forearm vascular resistance. Blood pressure averaged 124 +/- 3/62 +/- 2 mm Hg on the low sodium diet and 122 +/- 3/60 +/- 2 mm Hg on the high sodium diet (p = NS). Baroreceptor reflex slopes representing the systolic and diastolic blood pressure responses to changes in neck chamber pressure were steeper in the subjects when randomly assigned to low sodium diet than to high sodium diet. Diastolic blood pressure decay time and forearm arterial compliance were similar during low and high sodium intake. We conclude that short-term exposure to a high sodium diet depresses carotid baroreceptor reflex function in normotensive humans. This observation cannot be attributed to changes in the arterial compliance.

Full Text

Duke Authors

Cited Authors

  • Creager, MA; Roddy, MA; Holland, KM; Hirsch, AT; Dzau, VJ

Published Date

  • June 1991

Published In

Volume / Issue

  • 17 / 6 Pt 2

Start / End Page

  • 989 - 996

PubMed ID

  • 2045181

International Standard Serial Number (ISSN)

  • 0194-911X

Digital Object Identifier (DOI)

  • 10.1161/01.hyp.17.6.989


  • eng

Conference Location

  • United States