Microvascular Permeability after an Acute and Chronic Salt Load in Healthy Subjects

2018 ◽  
Vol 128 (2) ◽  
pp. 352-360 ◽  
Author(s):  
Nienke M. G. Rorije ◽  
Rik H. G. Olde Engberink ◽  
Youssef Chahid ◽  
Naomi van Vlies ◽  
Jan P. van Straalen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Surface Layer ◽  
Dietary Sodium ◽  
Endothelial Surface Layer ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Sodium Loading ◽  
Endothelial Surface ◽  
Transcapillary Escape Rate ◽  
Intravenous Sodium

Abstract Background Sodium-induced microcirculatory changes, endothelial surface layer alterations in particular, may play an important role in sodium-mediated blood pressure elevation. However, effects of acute and chronic sodium loading on the endothelial surface layer and microcirculation in humans have not been established. The objective of this study was to assess sodium-induced changes in blood pressure and body weight as primary outcomes and also in microvascular permeability, sublingual microcirculatory dimensions, and urinary glycosaminoglycan excretion in healthy subjects. Methods Twelve normotensive males followed both a low-sodium diet (less than 50 mmol/day) and a high-sodium diet (more than 200 mmol/day) for eight days in randomized order, separated by a crossover period. After the low-sodium diet, hypertonic saline (5 mmol sodium/liter body water) was administered intravenously in 30 min. Results Both sodium interventions did not change blood pressure. Body weight increased with 2.5 (95% CI, 1.7 to 3.2) kg (P < 0.001) after dietary sodium loading. Acute intravenous sodium loading resulted in increased transcapillary escape rate of 125I-labeled albumin (2.7 [0.1 to 5.3] % cpm · g−1 · h–1; P = 0.04), whereas chronic dietary sodium loading did not affect transcapillary escape rate of 125I-labeled albumin (−0.03 [−3.3 to 3.2] % cpm · g−1 · h–1; P = 1.00), despite similar increases of plasma sodium and osmolality. Acute intravenous sodium loading coincided with significantly increased plasma volume, as assessed by the distribution volume of albumin, and significantly decreased urinary excretion of heparan sulfate and chondroitin sulfate. These changes were not observed after dietary sodium loading. Conclusions Our results suggest that intravenous sodium loading has direct adverse effects on the endothelial surface layer, independent of blood pressure.

Development of two-kidney Goldblatt hypertension in rats under dietary sodium restriction

1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Goldblatt Hypertension

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.

Gastrointestinal control of sodium excretion in sodium-depleted conscious rabbits

1976 ◽  
Vol 230 (6) ◽  
pp. 1504-1508 ◽  
Author(s):  
RM Carey ◽  
Smith ◽  
EM Ortt
Keyword(s):  
Gastrointestinal Tract ◽  
Sodium Excretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Sodium Excretion ◽  
Sodium Loading ◽  
Conscious Rabbits ◽  
Intravenous Sodium ◽  
Oral Sodium

Recent studies of sodium-depleted rabbits have shown that oral sodium loading is followed by greater natriuresis than intravenous sodium loading. The present study was undertaken to determine if this is dependent on differences in aldosterone excretion. Rabbits in balance on a low-sodium diet were given bolus doses of sodium either orally or intravenously. Those receiving oral sodium responded with a greater natriuresis than those receiving it intravenously. No differences in aldosterone excretion were demonstrated after oral or intravenous sodium repletion. Rabbits given large doses of exogenous aldosterone continued to excrete more sodium after oral than after intravenous repletion. This study demonstrates that in rabbits the gastrointestinal tract functions to regulate renal sodium excretion and that the mechanism is independent of aldosterone.

Dietary Sodium Restriction in Normotensive Subjects and Patients with Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 399s-402s ◽  
Author(s):  
G. A. MacGregor ◽  
N. D. Markandu ◽  
G. A. Sagnella
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Normal Diet ◽  
Mean Blood Pressure ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Normotensive Subjects

1. Seventy-seven patients with essential hypertension and 28 normotensive subjects were studied on their normal diet (ND), on the fifth day of a high sodium diet (HS) (350 mmol/day) and on the fifth day of a low sodium diet (LS) (10 mmol/day). 2. With an increase in sodium intake, there was no change in mean blood pressure either in the normotensive subjects (ND, 120/75 ± 2.4/1.7 mmHg—HS, 119/75 ± 2.7/1.7 mmHg) or in the hypertensive subjects (ND, 173/110 ± 2.5/1.3 mmHg—HS, 174/110 ± 2.5/1.4 mmHg). 3. On the fifth day of the low sodium diet there was no change in mean blood pressure in the normotensive subjects (ND, 120/75 ± 2.5/1.7 mmHg—LS, 116/76 ± 2.7/2.0 mmHg). In contrast, the hypertensive group on the fifth day of the low salt diet had a significant fall in supine mean blood pressure compared with those on the normal diet (ND, 173/110 ± 2.5/1.3—LS, 155/102 ± 2.2/1.3 mmHg; P < 0.001). The fall in mean blood pressure was 10.8 ± 1.1 mmHg (8.4%). 4. There was a significant correlation between the fall in blood pressure with the low sodium diet and the level of blood pressure on the normal diet (r = 0.52; P < 0.001) and a significant inverse correlation with the fall in blood pressure on the low sodium diet and the rise in plasma renin activity from the normal to low sodium diet (r = −0.36; P < 0.001). 5. Nineteen patients with mild to moderate essential hypertension were studied in a double-blind randomized crossover study of moderate dietary sodium restriction using slow sodium and placebo for 1 month each. On the fourth week of placebo (mean 24 h UNa 86 ± 9 mmol), mean supine blood pressure was 7.1 mmHg lower (6.1%), P < 0.001 compared with the fourth week of slow sodium (mean 24 h UNa 162 ± 9 mmol). 6. Moderate dietary sodium restriction over 1 month caused a fall in blood pressure in patients with essential hypertension. A more severe reduction in sodium intake for a shorter period of time lowered blood pressure in hypertensive but not normotensive subjects. Part of the mechanism of this blood pressure reduction with sodium restriction appeared to be related to the severity of the hypertension and to suppression of the renin-angiotensin system.

Effect of sodium intake on gene expression and plasma levels of ANF in rats

1988 ◽  
Vol 255 (2) ◽  
pp. H245-H249
Author(s):  
A. L. Lattion ◽  
J. F. Aubert ◽  
J. P. Fluckiger ◽  
J. Nussberger ◽  
B. Waeber ◽  
...  
Keyword(s):  
Gene Expression ◽  
Plasma Levels ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Dot Blot ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Sodium Loading ◽  
High Sodium Diet

The effect of short- and long-term sodium loading and sodium restriction on the gene expression as well as on circulating plasma levels of atrial natriuretic factor (ANF) was evaluated in normotensive Wistar rats. These rats were fed either a low-, a regular-, or a high-sodium diet (regular diet and 1% saline as drinking fluid) and studied after 1 and 3 wk. The ANF mRNA was determined in pooled atria and ventricles of the different groups of rats, using the dot-blot technique. Plasma ANF levels were measured with a radioimmunoassay. After 1 wk on the high-sodium diet, ANF mRNA was increased in right atria and ventricles together with circulating ANF levels when compared with animals maintained for the same period on a low-sodium diet. After 3 wk on the various diets, the differences in cardiac ANF mRNA and in plasma ANF levels had disappeared. Gene expression of ANF was also looked for in different areas of the brain, lung, thyroid, adrenals, and the kidney; no hybridization was detected in any of these organs. These data suggest that in rats, the transcription of the ANF gene and peptide release in enhanced only during short-term adaptation to dietary sodium loading.

A Comparison of Natriuresis after Oral and Intravenous Sodium Loading in Sodium-Depleted Rabbits: Evidence for a Gastrointestinal or Portal Monitor of Sodium Intake

1975 ◽  
Vol 49 (5) ◽  
pp. 433-436 ◽  
Author(s):  
R. J. Lennane ◽  
W. S. Peart ◽  
R. M. Carey ◽  
J. Shaw
Keyword(s):  
Sodium Chloride ◽  
Sodium Intake ◽  
Portal Circulation ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sodium Loading ◽  
Portal Monitor ◽  
Oral Doses ◽  
Intravenous Sodium

1. Rabbits in balance on a low sodium diet were given doses of sodium chloride either orally or intravenously. 2. Those receiving oral doses responded with a much greater natriuresis than those receiving intravenous ones. 3. This could be explained by the existence of a sodium input monitor somewhere in the gut or portal circulation.

Contrasting endocrine responses to acute oral compared with intravenous sodium loading in normal humans

1998 ◽  
Vol 274 (1) ◽  
pp. F111-F119 ◽  
Author(s):  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Martin G. Buckley ◽  
Michelle A. Miller ◽  
Giuseppe A. Sagnella ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Fold Increase ◽  
Early Response ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Loading ◽  
Sodium Load ◽  
Intravenous Sodium ◽  
Oral Sodium

There is evidence in animals and in humans for accelerated natriuresis after oral compared with intravenous sodium loading. To assess the role of atrial natriuretic peptide (ANP) as a contributory mechanism, we compared the hormonal responses to an intravenous sodium load and to the same sodium load taken orally in three separate groups of healthy subjects in balance on low, normal, or high sodium intake. On each diet, there was a trend for an early delay in sodium excretion, followed by increased natriuresis after the oral compared with intravenous sodium load. On all levels of dietary sodium intake, there was a significant (∼2-fold) increase in plasma ANP levels after intravenous saline infusion. There was a significant suppression of the renin system both after oral and intravenous sodium loading. However, there was no acute increase in plasma ANP levels after the oral sodium load, except on the very low sodium intake. This striking and unexpected observation suggests that changes in plasma ANP levels appear to play little role in the early response to an acute oral sodium load in subjects with sodium intake in the range of 150–350 mmol/day. Endocrine mechanisms for the accelerated increase in sodium excretion after oral compared with intravenous sodium loading remain to be elucidated.

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