SUMMARY Fifty-eight normal subjects and 51 subjects with borderline hypertension underwent microvascular and hemodynamic studies while on an ad libitum diet and during periods of sodium depletion (10 mEq/day) and repletion (200 mEq/day). Hemodynamic measurements included arterial blood pressure, cardiac index, total peripheral resistance, forearm blood flow, vascular resistance, venous compliance, and capillary filtration fraction. Studies of the mlcrocirculation consisted of macrophotography of the buibar conjunctiva with measurement of anteriolar, venular, and capillary density and diameter. During sodium repletion, cardiac index increased significantly in the normal subjects (2.35 ± 0.7 vs 2.44 ± 0.7 L/min/m 2 ; p<0.01) and in the borderline hypertensive subjects (2.50 ± 0.7 vs 2.70 ± 0.8 L/min/m 2 ; p<0.01). However, mean blood pressure rose by more than 5% in only 33 subjects, 13 with normal and 20 with borderline hypertension. When these sodium-sensitive subjects were compared with those whose blood pressure did not rise, the former were found to have significantly higher forearm vascular resistance (32.2 ± 21 vs 17.9 ± 12 mm Hg/ml/min/lOOg; p<0.01), lower forearm blood flow (4.42 ± 2.7 vs 7.47 ± 5.0 ml/min/100 g) and lower conjunctival capillary density (3.72 ± 1.7 vs 5.18 ±2.1 [SD] mm/mm 2 ; p< 0.05). These results indicate that sodium sensitivity In humans is accompanied by elevation of forearm vascular resistance and attenuation of the microcirculatton. (Hypertension 9: 398-406, 1987) KEY WORDS • hypertension microcirculation sodium • vascular resistance * hemodynamics T HE conclusion that certain individuals are sodium-sensitive is supported by two main lines of evidence, experimental and epidemiological. Meneely et al. 1 found that rats fed a high sodium diet displayed a wide spectrum of blood pressure responses: some became severely hypertensive, some remained normotensive, and others manifested intermediate levels of blood pressure elevation. After several generations of selective inbreeding, Dahl et al. were able produce strains of genetically sodium-sensitive and sodium-resistant rats. Received December 16, 1985; accepted December 10, 1986. While studies within populations have not shown a direct relationship between individual sodium intake and blood pressure, possibly because of a saturation effect, studies of human populations have also supported the concept of individual susceptibility to the hypertensive effects of sodium. Several surveys have demonstrated a positive relationship between sodium intake and the prevalence of hypertension.3 However, normotensive persons can be found even in populations ingesting large quantities of sodium, suggesting that some humans are sodium-resistant while others are sodium-sensitive. 4 A number of investigators have observed abnormalities in the vascular resistance of patients with early, mild hypertension that might underlie sodium sensitivity. "12 The purpose of the present study was to identify persons whose blood pressure rises with increases in ...

No abstract

SUMMARY The long-term hemodynamic effects of a high dietary sodium intake were studied in 10 young normal subjects. After a 4-day diet of 10 mEq of sodium and 60 mEq of potassium per day the mean arterial blood pressure (MAP) was 82.3 ± 15.1 mm Hg, the cardiac index ( 1 -2 However, in areas with an exceptionally high sodium intake, the majority of individuals remain free of hypertension.3 One model of essential hypertension proposes that certain individuals are born with a genetic predisposition 4 which, when combined with a diet containing added sodium, leads to renal retention of sodium and water, and expansion of plasma and extracellular fluid volume with increased cardiac output. 5 Chronic increase in cardiac output might stimulate autoregulation in the various tissues of the body leading to increased total peripheral resistance and increased blood pressure. However, normotensive individuals who do not restrict sodium must be able to circumvent this sequence of events. Our objectives were to identify individuals whose arterial blood pressure did not rise in response to sodium repletion over a

SUMMARY To investigate factors associated with sodium sensitivity, 157 subjects were studied while receiving 10 and 200 mEq sodium diets. Measurements included blood pressure (BP), forearm vascular resistance, plasma renin activity (PRA), and plasma aldosterone. Sodium repletion was associated with a greater than 5% increase in mean BP in 16% of the normotensive subjects and 29% of the borderline hypertensive subjects. Sodium-sensitive subjects were compared with sodiumresistant subjects in both the normotensive (n = 92) and borderline hypertensive (n = 65) groups. Forearm vascular resistance was significantly higher (p<0.05) during sodium loading in the sodiumsensitive subgroups of both the normotensive and borderline hypertensive groups (35.8 ± 29 vs 23.8 ± 20 [SD] and 37.5 ± 29 vs 22.5 ± 14 mm Hg/ml/min/100 g, respectively. Venous capacitance was lower in the sodium-sensitive than in the sodium-resistant borderline hypertensive subjects (0.8 ± 0.21 vs 1.69 ± 0.24 ml/100 g). During sodium restriction, PRA was significantly lower (p<0.01) in the sodium-sensitive subsets (2.56 ± 1.6 vs 4.04 ± 2.6; 2.65 ± 2.1 vs 3.88 ± 2.6 ng angiotensin I/ml/hr). Aldosterone was lower (p<0.01) during sodium depletion in the sodium-sensitive subsets (17.3 ± 12 vs 26.3 ± 16; 18.5 ± 18 vs 27.9 ± 17 ng/ml). A significant inverse correlation existed between change in BP with sodium repletion and change in PRA or level of PRA during sodium depletion (p<0.003). We conclude that both normotensive and borderline hypertensive sodiumsensitive subjects are characterized by an increase in forearm vascular resistance during high sodium intake and that this characteristic is associated with decreased responsiveness of the renin-aldosterone system during sodium depletion. (Hypertension 11: 717-723, 1988) KEY WORDS * hypertension • sodium • vascular resistance • hemodynamics renin • aldosterone A LTHOUGH considerable evidence links dietary / \ sodium intake with high blood pressure, sev-A. \ . eral observations suggest that all persons are not affected equally by the hypertensive effects of sodium. By selective inbreeding, Dahl et al.1 have developed strains of rats that become hypertensive when fed a high sodium diet and others that are resistant to the hypertensive effects of sodium. Worldwide studies of sodium intake in various human populations have shown a direct relationship between sodium intake and the prevalence of hypertension, 2 yet in certain populations, the majority of persons remain normotensive despite high sodium intake.3 Over the past several years, a number of investigators have demonstrated

No abstract