Excessive sodium retention as a characteristic of salt-sensitive hypertension

Am J Med Sci. 1986 Aug;292(2):67-74. doi: 10.1097/00000441-198608000-00001.


To investigate the possibility that salt-sensitive hypertensives have deficient sodium excretion, the sodium retained by 20 hypertensive patients during a salt load (SL = 3.88 mEq/Kg/day) was calculated for 3 days immediately after 4 days of sodium deprivation (SD = 9 mEq/d). Patients were divided into two groups by arterial pressure responses to SD: responders (N = 10) whose pressures became normal rapidly and averaged less than 140/90 during SD and nonresponders (n = 10) whose pressures were not affected. Sodium retention (mEq/Kg) during SL was calculated as cumulative sodium intake minus cumulative urinary sodium divided by body weight. Responders retained more sodium during SL than nonresponders (3.71 +/- 0.96 [SD] vs. 2.52 +/- 1.05 mEq/Kg, p less than 0.02). This could not be explained by a measurable decrease in filtered sodium load since creatinine clearance was the same in each group. Neither was it associated with differences in plasma renin activity (PRA) or aldosterone excretion rates (AER). Whereas PRA was significantly lower in responders at the end of SD, AER was not different; with SL, group values were equally suppressed. Also sodium excretion was not correlated with arterial pressure except in non-responders on the last day of SL. These data indicate that salt-sensitive hypertensives handle sodium differently than nonsalt-sensitive hypertensives.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Aldosterone / urine
  • Blood Pressure / drug effects
  • Blood Volume / drug effects
  • Body Weight
  • Creatinine / urine
  • Female
  • Humans
  • Hypertension / metabolism*
  • Male
  • Middle Aged
  • Natriuresis / drug effects
  • Renin / blood
  • Renin-Angiotensin System / drug effects
  • Sodium / metabolism*
  • Sodium / pharmacology


  • Aldosterone
  • Sodium
  • Creatinine
  • Renin