Chronic activation of brain areas by high-sodium diet in Dahl salt-sensitive rats

1998 ◽  
Vol 274 (6) ◽  
pp. H2046-H2052 ◽  
Author(s):  
Adam S. Budzikowski ◽  
Faranak Vahid-Ansari ◽  
Frans H. H. Leenen
Keyword(s):  
Sodium Intake ◽  
Brain Areas ◽  
Hypothalamic Area ◽  
High Sodium ◽  
Sodium Diet ◽  
Transient Activation ◽  
Nucleus Of Solitary Tract ◽  
Central Gray ◽  
High Sodium Diet

To map changes in neuronal activity in the brains of Dahl salt-sensitive (Dahl S) vs. salt-resistant (Dahl R) rats by high-sodium diet, we used immunohistochemical detection of Fra-like proteins as a marker for long-term neuronal activation. Compared with Dahl R rats during regular sodium intake, Dahl S rats showed modestly higher expression of Fra-like immunoreactivity (Fra-LI) in the supraoptic nucleus, anterior hypothalamic area (AHA), central gray, and nucleus of solitary tract (NTS) at 5, 6, and 9 wk of age but clearly elevated Fra-LI in the magnocellular part of the paraventricular nucleus (PVN) at 6 wk of age (but not at 5 and 9 wk). In the median preoptic nucleus (MnPO) Fra-LI was lower at 9 wk of age and no differences were observed in the parvocellular PVN and subfornical organ in Dahl S vs. Dahl R rats on regular sodium intake. Compared with Dahl S rats on a regular-sodium diet, Dahl S rats on a high-sodium diet from 4 to 9 wk of age had significantly increased blood pressure and experienced transient activation of magnocellular PVN and MnPO and virtually no changes in the activity of the parvocellular PVN, AHA, and NTS. In contrast, Dahl R rats showed marked activation in the magnocellular PVN after 1 and 2 wk on a high-sodium diet compared with Dahl R rats on a regular-sodium diet. The present study demonstrates that Dahl S rats show differential activation of brain areas participating in regulation of osmotic and cardiovascular homeostasis during development of sodium-sensitive hypertension.

scholarly journals Sodium Intake and Heart Failure

2020 ◽  
Vol 21 (24) ◽  
pp. 9474
Author(s):  
Yash Patel ◽  
Jacob Joseph
Keyword(s):  
Heart Failure ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Mechanical Performance ◽  
Sodium Intake ◽  
Heart Association ◽  
Dietary Practices ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure.

scholarly journals Dietary sodium modulates the interaction between efferent and afferent renal nerve activity by altering activation of α2-adrenoceptors on renal sensory nerves

2011 ◽  
Vol 300 (2) ◽  
pp. R298-R310 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Saku Ruohonen ◽  
Mika Scheinin ◽  
...  
Keyword(s):  
Substance P ◽  
Sodium Intake ◽  
Sensory Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Renal Nerve Activity ◽  
High Sodium Diet

Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which then reflexively decreases ERSNA via activation of the renorenal reflexes to maintain low ERSNA. The ERSNA-ARNA interaction is mediated by norepinephrine (NE) that increases and decreases ARNA by activation of renal α1-and α2-adrenoceptors (AR), respectively. The ERSNA-induced increases in ARNA are suppressed during a low-sodium (2,470 ± 770% s) and enhanced during a high-sodium diet (5,670 ± 1,260% s). We examined the role of α2-AR in modulating the responsiveness of renal sensory nerves during low- and high-sodium diets. Immunohistochemical analysis suggested the presence of α2A-AR and α2C-AR subtypes on renal sensory nerves. During the low-sodium diet, renal pelvic administration of the α2-AR antagonist rauwolscine or the AT1 receptor antagonist losartan alone failed to alter the ARNA responses to reflex increases in ERSNA. Likewise, renal pelvic release of substance P produced by 250 pM NE (from 8.0 ± 1.3 to 8.5 ± 1.6 pg/min) was not affected by rauwolscine or losartan alone. However, rauwolscine+losartan enhanced the ARNA responses to reflex increases in ERSNA (4,680 ± 1,240%·s), and renal pelvic release of substance P by 250 pM NE, from 8.3 ± 0.6 to 14.2 ± 0.8 pg/min. During a high-sodium diet, rauwolscine had no effect on the ARNA response to reflex increases in ERSNA or renal pelvic release of substance P produced by NE. Losartan was not examined because of low endogenous ANG II levels in renal pelvic tissue during a high-sodium diet. Increased activation of α2-AR contributes to the reduced interaction between ERSNA and ARNA during low-sodium intake, whereas no/minimal activation of α2-AR contributes to the enhanced ERSNA-ARNA interaction under conditions of high sodium intake.

Impact of elevated dietary sodium intake on NAD(P)H oxidase and SOD in the cortex and medulla of the rat kidney

2010 ◽  
Vol 299 (1) ◽  
pp. R234-R240 ◽  
Author(s):  
Edward J. Johns ◽  
Barbara O'Shaughnessy ◽  
Susan O'Neill ◽  
Bríd Lane ◽  
Vincent Healy
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Oxidase Activity ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Renal Diseases ◽  
Water Excretion ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

Pathophysiological states, including cardiovascular and renal diseases, are characterized by oxidative stress but what is less clear is whether physiological challenges incur a degree of altered oxidative metabolism. To this end, this study examined whether exposure to a high dietary sodium intake could cause an oxidative stress at the kidney. Animals, placed on either 0.3% or 3% sodium diets for 2 wk, were given a lethal dose of anesthetic, and kidneys were removed to analyze both NAD(P)H oxidase (NOX) and superoxide dismutase (SOD) expression and activities in the cortex and medulla. Placing animals on the high-sodium diet raised sodium and water excretion and caused an ∼14-fold increase in urinary excretion of 8-isoprostane, a marker of oxidative stress, which was attenuated by chronic treatment with apocynin to prevent NAD(P)H oxidase activity. The protein expression of the NAD(P)H oxidase subunits NOX2 and p47phox and overall NAD(P)H oxidase activity were approximately doubled in the cortex of the rats on the high-sodium diet compared with those on the normal sodium intake while both SOD activity and expression were unchanged. By contrast, neither NOX nor SOD protein expression or activity were altered in the medulla when the rats were placed on the high-sodium intake. These data suggest that an elevation in dietary sodium intake can lead to increased generation of reactive oxygen species and a state of oxidative stress in the cortex but not to such a degree that it extends to the medulla.

Plasma Angiotensin II Concentration Regulates Vascular but Not Adrenal Responsiveness to Restriction of Sodium Intake in Normal Man

1981 ◽  
Vol 61 (5) ◽  
pp. 527-534 ◽  
Author(s):  
Bess F. Dawson-Hughes ◽  
T. J. Moore ◽  
R. G. Dluhy ◽  
N. K. Hollenberg ◽  
G. H. Williams
Keyword(s):  
Sodium Intake ◽  
Regression Line ◽  
Sodium Balance ◽  
Ang Ii ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Intake ◽  
Low Sodium ◽  
Vascular Responsiveness ◽  
High Sodium Diet

1. Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). These responses may be mediated either by the circulating level of ANG II or other mechanisms also modified by a change in sodium balance. To assess the importance of the ANG II level, captopril, an oral converting enzyme inhibitor, was used to lower the plasma ANG II level to the sodium-loaded range while maintaining subjects in low sodium balance. 2. Normal volunteer subjects received an infusion of ANG II in increasing doses in three states: high sodium intake, low sodium intake and low sodium intake after pretreatment with captopril. 3. Basal levels of ANG II on high-sodium diet and low-sodium diet plus captopril were similar. In the ANG II infusion studies the slope of the aldosterone—ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. After the addition of captopril the slope was not decreased, indicating that the endogenous ANG II concentration is not necessary to maintain adrenal sensitivity during sodium restriction. 4. In the ANG II infusion studies the slope of the mean blood pressure—ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. The addition of captopril to sodium-restricted subjects caused the slope of the regression relationship to increase significantly, consistent with an enhanced vascular responsiveness when endogenous ANG II levels were lowered. However, the slope on low sodium plus captopril did not increase to the level of subjects on a high-sodium diet, suggesting that factors in addition to the circulating ANG II level are also important in regulating the vascular responsiveness to ANG II.

scholarly journals Sex differences in salt sensitivity to nitric oxide dependent vasodilation in healthy young adults

2012 ◽  
Vol 112 (6) ◽  
pp. 1049-1053 ◽  
Author(s):  
John H. Eisenach ◽  
Leah R. Gullixson ◽  
Susan L. Kost ◽  
Michael J. Joyner ◽  
Stephen T. Turner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
No Production ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Before And After ◽  
High Sodium Diet

Dietary sodium and blood pressure regulation differs between normotensive men and women, an effect which may involve endothelial production of nitric oxide (NO). Therefore, we tested the hypothesis that differences in the NO component of endothelium-dependent vasodilation between low and high dietary sodium intake depend on sex. For 5 days prior to study, healthy adults consumed a controlled low-sodium diet (10 mmol/day, n = 30, mean age ± SE: 30 ± 1 yr, 16 men) or high-sodium diet (400 mmol/day, n = 36, age 23 ± 1 yr, 13 men). Forearm blood flow (FBF, plethysmography) responses to brachial artery administration of acetylcholine (ACh, 4 μg·100 ml tissue−1·min−1) were measured before and after endothelial NO synthase inhibition with NG-monomethyl-l-arginine (l-NMMA, 50 mg bolus + 1 mg/min infusion). The NO component of endothelium-dependent dilation was calculated as the response to ACh before and after l-NMMA accounting for changes in baseline FBF: [(FBF ACh − FBF baseline) − (FBF AChL-NMMA − FBF baselineL-NMMA)]. This value was 5.7 ± 1.3 and 2.5 ± 0.8 ml·100 ml forearm tissue−1·min−1 for the low- and high-sodium diets, respectively (main effect of sodium, P = 0.019). The sodium effect was larger for the men, with values of 7.9 ± 2.0 and 2.2 ± 1.4 for men vs. 3.1 ± 1.3 and 2.7 ± 1.0 ml·100 ml forearm tissue−1·min−1 for the women ( P = 0.034, sex-by-sodium interaction). We conclude that the NO component of endothelium-dependent vasodilation is altered by dietary sodium intake based on sex, suggesting that endothelial NO production is sensitive to dietary sodium in healthy young men but not women.

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.

Influence of sodium intake on in vivo left ventricular anatomy in experimental renovascular hypertension

1993 ◽  
Vol 264 (6) ◽  
pp. H2103-H2110 ◽  
Author(s):  
G. de Simone ◽  
R. B. Devereux ◽  
M. J. Camargo ◽  
D. C. Wallerson ◽  
J. H. Laragh
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Sodium Content ◽  
Left Ventricular ◽  
Dietary Sodium ◽  
Area Index ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

The effect of different dietary salt contents (0.0035, 0.4, and 4%) on in vivo left ventricular (LV) geometry was studied by necropsy-validated echocardiographic methods in groups of 30 two-kidney, one-clip (2K, 1C) and one-kidney, one-clip (1K, 1C) male Wistar rats and two-kidney (2K) and one-kidney (1K) shams 9 wk after surgery. The salt-deficient diet was associated with lower body weight, higher plasma renin activity in both 2K,1C and 2K shams (P < 0.004) and higher hematocrit in 2K,1C (P < 0.02). Blood pressure was increased by high-salt diet in experimental groups but not in shams (P < 0.01). Increase in dietary sodium content was associated with increased cross-sectional area index (CSAI) and LV mass index in 2K rats independently of renal artery stenosis (P < 0.0007) and also in 1K shams (P < 0.01). LV end-diastolic dimension was greater in 1K,1C and 1K shams than in 2K,1C and 2K shams at every level of sodium intake and was directly related to atrial natriuretic factor levels in both 1K,1C (r = 0.68) and 2K,1C (r = 0.59). LV hypertrophy was independently predicted by blood pressure (P < 0.0006) and high-sodium diet (P < 0.05) in 1K rats (multiple r = 0.57, P < 0.001) and by high-sodium diet (P < 0.0001) and low hematocrit (P < 0.05) in 2K rats (multiple r = 0.76, P < 0.0001). Thus provision of normal or high sodium content in the diet was a more consistent stimulus to LV hypertrophy than the level of blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of dietary sodium intake on the pressor reactivity to angiotensin II in rats with experimental cirrhosis of the liver

1989 ◽  
Vol 67 (12) ◽  
pp. 1506-1511 ◽  
Author(s):  
L. M. Villamediana ◽  
Angel L. García-Villalón ◽  
Carlos Caramelo ◽  
José M. López-Novoa
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Reactivity ◽  
Sodium Intake ◽  
Pressor Response ◽  
Experimental Cirrhosis ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

The present experiments were designed to evaluate vascular reactivity to angiotensin II in rats with experimental cirrhosis of the liver (induced with CCl4 and phenobarbital) before ascites appearance. The systemic pressor response to angiotensin II in conscious animals and the contractile effect of angiotensin II in isolated femoral arteries were studied. In addition, the effect of high sodium intake on these parameters was also analyzed. Both renin and aldosterone plasma concentrations were similar in control and cirrhotic rats on the normal or on the high sodium diet. Basal mean arterial pressure was higher in control rats than in cirrhotic rats on the normal sodium (116 ± 4 vs. 101 ± 4 mmHg (1 mmHg = 133.3 Pa),p < 0.05) or on the high sodium diet (118 ± 7 vs. 98 ± 6 mmHg). No differences in plasma renin activity or plasma aldosterone were found between control and cirrhotic rats. Upon injection of angiotensin II, control rats show a dose-dependent increase in mean arterial pressure which is higher in high sodium than in normal sodium rats. Cirrhotic rats showed a lower hypertensive response to angiotensin II than their corresponding control rats. In addition, no difference between pressor responses to angiotensin II was observed when normal sodium and high sodium cirrhotic rats were compared. On application of angiotensin II, femoral arteries of control and cirrhotic rats exhibited a dose-dependent contraction. However, maximal contraction was higher in high sodium control rats (145 ± 12 mg) than in normal sodium control rats (99 ± 6 mg, p < 0.05). No significant differences between control and cirrhotic rats on either sodium diet were observed. In conclusion, cirrhotic, nonascitic rats showed an impaired pressor response to angiotensin II that is more marked after a high sodium diet. These differences are not due to changes in the contractility of peripheral arteries to angiotensin II.Key words: angiotensin II, liver cirrhosis, sodium intake, mean arterial pressure, vascular reactivity.

Sign in / Sign up

Export Citation Format

Share Document