Effect of sodium intake on blood pressure, serum levels and renal excretion of sodium and potassium in normotensives with and without familial predisposition to hypertension.
1. Seventeen normal volunteers aged 19 to 22 were randomly subjected, in a trial of crossover design, to three distinct regimens of sodium chloride intake: high (16 to 20 g), normal (8 to 12 g) and low (0.5 to 1 g). Each regimen lasted nine days, with determination of blood pressure and heart rate (in the supine position and after sudden rising), body weight, and urinary output of creatinine, sodium and potassium on the third, sixth and ninth days. In addition, plasma levels of creatinine, sodium and potassium were determined on the ninth day so that sodium and potassium clearance and fractional excretion could be calculated. 2. Eleven of the volunteers had a family history of hypertension. Compared to the six without such a history, these subjects showed: 1) higher supine systolic blood pressure on the third day of sodium overload (124.7 +/- 3.0 vs 112.3 +/- 2.9 mmHg, P less than 0.02); 2) higher supine diastolic blood pressure on the third day of sodium overload (76.5 +/- 2.8 vs 64.5 +/- 4.3 mmHg; P less than 0.05); 3) higher supine diastolic blood pressure on the sixth day of sodium overload (73.7 +/- 2.3 vs 63.8 +/- 3.2 mmHg, P less than 0.05); 4) lower supine heart rate on the ninth day of sodium overload (61.0 +/- 3.1 vs 72.7 +/- 4.6, P less than 0.05), and 5) lower plasma potassium on the ninth day of sodium overload (4.10 +/- 0.05 vs 4.28 +/- 0.06 mEq/l, P less than 0.05). 3. These results suggest that normal individuals whose familial history places them at risk for the development of hypertension differ from those not at risk during their adaptation to sodium load by suffering a transient elevation of blood pressure within a few days of the increase in load. The low levels of plasma potassium observed in these volunteers after a period of sodium load may be due to the operation of different renal mechanisms of sodium excretion in this group, leading to increased kaliuresis, and may explain the high vascular reactivity of such individuals.
Fuchs
F D
FD
Departamento de Fisiologia, Farmacologia e Biofísica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil.
Wannmacher
C M
CM
Wannmacher
L
L
Guimarães
F S
FS
Rosito
G A
GA
Gastaldo
G
G
Hoeffel
C P
CP
Wagner
E M
EM
D000328:Adult; D001794:Blood Pressure / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D003404:Creatinine / Q000493:pharmacokinetics; D004032:Diet; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000235:genetics*; D008297:Male; D011188:Potassium / Q000652:urine*; D011897:Random Allocation; D012307:Risk Factors; D012964:Sodium / Q000652:urine*; D012965:Sodium Chloride / Q000494:pharmacology*
D012965:Sodium Chloride; D012964:Sodium; D003404:Creatinine; D011188:Potassium