Elevation of Morning Blood Pressure in Sodium Resistant Subjects by High Sodium Diet

The present study evaluated the response of blood pressure (BP) by dietary sodium in sodium resistant (SR) subjects. One hundred one subjects (mean age, 46.0 yr; 31 hypertensives) were admitted and given low sodium-dietary approaches to stop hypertension (DASH) diet (LSD, 100 mM NaCl/day) for 7 days and high sodium-DASH diet (HSD, 300 mM NaCl/day) for the following 7 days. On the last day of each diet, 24 hr ambulatory BP was measured. Morning systolic BP (SBP) and diastolic BP (DBP) were elevated after HSD in all subjects (P 0.05). In hypertensive subjects, morning DBP elevation was greater than daytime DBP elevation (P = 0.036), although both DBPs were significantly elevated after HSD. The augmented elevation of morning DBP in hypertensive subjects was contributed by the absolute elevation of morning DBP (P = 0.032) and relative elevation to daytime DBP (P = 0.005) in sodium resistant (SR) subjects, but not by sodium sensitive subjects. Although there was no absolute elevation, SR subjects with normotension showed a relative elevation of morning SBP compared to daytime SBP change after HSD (P = 0.009). The present study demonstrates an absolute and relative elevation of morning BP in SR subjects by HSD.

Matching salt intake to physiological need in rats using foraging protocols

Several studies of the quantitative relationship between sodium need and sodium intake in rats are reviewed. Using acute diuretic treatment 24 h beforehand, intake matches need fairly accurately when intake is spread out in time by using a hypotonic solution of NaCl. In contrast, using a hypertonic solution, intake is typically double the need. Using the same diuretic treatment, although the natriuresis occurs within ~1 h, the appetite appears only slowly over 24 h. Increased plasma levels of aldosterone parallel the increased intake; however, treatment with metyrapone blocks the rise in aldosterone but has no effect on appetite. Satiation of sodium appetite was studied in rats using sodium loss induced by chronic diuretic treatment and daily salt consumption sessions. When a simulated foraging cost was imposed on NaCl access in the form of a progressive ratio lever press task, rats showed satiation for NaCl (break point) after consuming an amount close to their estimated deficit. The chronic diuretic regimen produced hypovolemia and large increases in plasma aldosterone concentration and renin activity. These parameters were reversed to or toward non-depleted control values at the time of behavioral satiation in the progressive ratio protocol. Satiation mechanisms for sodium appetite thus do appear to exist. However, they do not operate quantitatively when concentrated salt is available at no effort, but instead allow overconsumption. There are reasons to believe that such a bias toward overconsumption may have been beneficial over evolutionary time, but such biasing for salt and other commodities is maladaptive in a resource-rich environment.

Dietary sodium intake and cardiac nerve cell hypertrophy in Wistar rats

We determined the effect of dietary sodium intake (0.15 and 8 per cent NACl) on the cardiac neuron size of normotensive 3-week old Wistar rats. An increase in dietary sodium for 48 weeks induced an increase in neuronal size. The number of large neurons (larger than 500 muM2) increased significantly (chi-square test) in rats ingesting 8 per cent NaCl in their food. The rats presented hypertension (128 ñ 9 vs 134 ñ 16 mmHg; difference not significant, Student t-test) and a statistically significant increase in cardiac muscle mass (1.6 ñ 0.1 vs 2.0 ñ 0.2 mg/g of rat). We conclude that food sodium can significantly increase cardiac nerve cell size and this trophic response occurs concomitantly with an increase of cardiac muscle mass.

Effect of dietary salt (NaCl) supplementation on urinary profile of guinea pigs (Cavia porcellus).

Sodium chloride supplementation (120 mg/kg of body weight/day) for 12 days increased the urinary excretion of calcium from 91.6 +/- 9.0 to 159.4 +/- 16.0 mumol/day and of sulphate from 266.8 +/- 24.5 to 1176.9 +/- 87.2 mumol/day in guinea pigs. The stone risk due to increased urinary calcium excretion could possibly be counterbalanced by increasing urinary sulphate excretion. High salt intake, thus, could not increase the risk of stone formation.

La endemia bociogena en la Republica Argentina: estudios epidemiologicos antes (1968) y durante (1986) la profilaxis con sal yodada en la ciudad de Buenos Aires / Endemic goiter in Argentina epidemiologic studies before (1968) and during (1986) prophylaxis with iodine salt in the city of Buenos Aires

Se presentan los resultados de dos encuestas de bocio efectuadas en Buenos Aires, una en 1968, anterior a la prifilaxis con sal yodada y la otra en 1986, durante su aplicación. La prevalencia de bocio fue de 14,8% y 8.5% respectivamente, siendo estadísticamente significativa la diferencia. La medida de las yodurias pasó de 92,7 µg/24 hs a 139,6 µg/g creatinina. Otros parámetros tiroides muestran diferencias definidas, indicando todos mayor contenido de yodo en el organismo. En 1968 había una asociación estadísticamente definida entre bocio y el nivel social del alumnado, que era de 6,8% en el alto, 12,2% en el medio y 26,4% en el bajo; en 1986 no se halló diferencia por nivel social. Tampoco se halló diferencia por sexo, pero se halló correlación con la edad, en ambas encuestas

High salt intake increases the vasorelaxant effect of anf on the isolated perfused rat kidney

1. The objetve of the present study was to determine whether chronic salt load or depletion leads to adaptive changes in Kinetics of atrial natriuretic factor (ANF) binding and/or responsiveness to ANF. We measured the equilibrium binding and the stead-state dose response effects of ANF1-28 on isolated kidneys from rats kept on a high (H) or low (L) salt diet for 15 days. 2. Twenty-four sodium excretion was 5.90 ñ 0.46 mEq for H vs 0.06 ñ 0.01 mEq for L(P<0.01). Plasma levels of immunoreactive ANF for H (42.2 ñ 3.9pg/ml) were not significantly different from those for L (35.2 ñ 5.3 pg/ml). s. There were no significant differences in distribution, apparent density or affinity of ANF specific binding sites determined in non-filtering isolated kidneys from rats kept on the H or L salt diet. 4. Dose-response curvas for the hemodynamic and excretory effects of ANF1-28 in filterin isolated kidneys from rats kept on the H salt diet were not different from those of rats kept on the L salt diet. In contrast, the vasorelaxant response to ANF 1-28 in isolated kidneys preconstricted by adding serum from 24-h nephrectomized rats to the prefusate (generation of angiotensin II) was significantly more pronounced in kidneys from ratas chronically adapted to the high-salt diet. 5. This effect of ANF may contribute to the increased renal plasma flow and glomerular filtration rate occuring under conditions of chronic salt loading in intact animals