Hemodynamic mechanisms of adaptation to chronic high sodium intake in normal humans.

摘要

The long-term hemodynamic effects of a high dietary sodium intake were studied in 10 young normal subjects. After a 4-day diet of 10mEq of sodium and 60 mEq of potassium per day the mean arterial blood pressure (MAP) was 82.3 +/- 15.1 mmHg, the cardiac index (CI) was 2.32 +/- 0.69 liter/min/m2, and total peripheral resistance (TPR) was 1778 +/- 947 dyne sec cm-5. After 4 to 6 days of 200 mEq of sodium and 60 mEq of potassium per day, MAP was 84.3 +/- 20.9 mm Hg, CI had risen to 2.53 +/- 0.61 liter/min/m2, and TPR fell to 1437 +/- 328 dyne sec cm-5. After 6 months of unrestricted sodium intake, urinary sodium excretion (UNa) was 144.1 +/- 51.9 mEq/24 hrs (p less than 0.001), MAP remained at 83.1 +/- 13.8 mm Hg, CI had risen to 3.11 +/- 1.01 liter/min/m2 (p less than 0.05) and TPR was 1268 +/- 444 dyne sec cm-5. After 12 months, UNa had risen to 171.5 +/- 97.6 mEq/24 hrs (p less than 0.005), while MAP remained at 82.4 +/- 17.9 mm Hg, CI at 3.08 +/- 1.16 liter/min/m2 (p less than 0.05), and TPR at 1282 +/- 500 dyne/sec/cm-5. Thus, cardiac index rises significantly with sodium intake in normal subjects and remains at a higher level for as long as 12 months. Blood pressure does not rise because TRP falls proportionately.