scholarly journals Age-related decrease of the chorda tympani nerve terminal field in the nucleus of the solitary tract is prevented by dietary sodium restriction during development

Neuroscience ◽  
2006 ◽  
Vol 137 (4) ◽  
pp. 1229-1236 ◽  
Author(s):  
S.I. Sollars ◽  
B.R. Walker ◽  
A.K. Thaw ◽  
D.L. Hill
Keyword(s):  
Nerve Terminal ◽  
Dietary Sodium ◽  
Chorda Tympani ◽  
Solitary Tract ◽  
Sodium Restriction ◽  
Chorda Tympani Nerve ◽  
Age Related ◽  
Dietary Sodium Restriction

scholarly journals Attenuation of peripheral salt taste responses and local immune function contralateral to gustatory nerve injury: effects of aldosterone

2009 ◽  
Vol 297 (4) ◽  
pp. R1103-R1110 ◽  
Author(s):  
Nick A. Guagliardo ◽  
Katie Nicole West ◽  
Lynnette P. McCluskey ◽  
David L. Hill
Keyword(s):  
Functional Results ◽  
Dietary Sodium ◽  
Chorda Tympani ◽  
Sodium Restriction ◽  
Chorda Tympani Nerve ◽  
Sodium Deficiency ◽  
Sodium Salts ◽  
Macrophage Response ◽  
Gustatory Nerve ◽  
Dietary Sodium Restriction

Dietary sodium restriction coupled with axotomy of the rat chorda tympani nerve (CTX) results in selectively attenuated taste responses to sodium salts in the contralateral, intact chorda tympani nerve. Converging evidence indicates that sodium deficiency also diminishes the activated macrophage response to injury on both the sectioned and contralateral, intact sides of the tongue. Because a sodium-restricted diet causes a robust increase in circulating aldosterone, we tested the hypothesis that changes in neurophysiological and immune responses contralateral to the CTX could be mimicked by aldosterone administration instead of the low-sodium diet. Taste responses in rats with CTX and supplemental aldosterone for 4–6 days were similar to rats with CTX and dietary sodium restriction. Responses to sodium salts were as much as 50% lower compared with sham-operated and vehicle-supplemented rats. The group-related functional differences were eliminated with lingual application of amiloride, suggesting that a major transduction pathway affected was through epithelial sodium channels. Consistent with the functional results, few macrophages were observed on either side of the tongue in rats with CTX and aldosterone. In contrast, macrophages were elevated on both sides of the tongue in rats with CTX and the vehicle. These results show that sodium deficiency or administration of aldosterone suppresses the immune response to neural injury, resulting in attenuation of peripheral gustatory function. They also show a potential key link among downstream consequences of sodium imbalance, taste function, and immune activity.

Novel regulation of peripheral gustatory function by the immune system

1996 ◽  
Vol 271 (4) ◽  
pp. R857-R862 ◽  
Author(s):  
L. M. Phillips ◽  
D. L. Hill
Keyword(s):  
Immune System ◽  
Dietary Sodium ◽  
Chorda Tympani ◽  
Sodium Restriction ◽  
Chorda Tympani Nerve ◽  
Nerve Section ◽  
Adult Rats ◽  
Systemic Injection ◽  
Gustatory Function ◽  
Dietary Sodium Restriction

Soon after adult rats receive unilateral chorda tympani nerve section in combination with dietary sodium restriction, neural taste responses recorded from the intact, contralateral chorda tympani nerve are substantially reduced. We hypothesized that the immune system is compromised in sodium-restricted rats, which leads to functional alterations in the peripheral taste system after neural injury. Here, immune function was stimulated with a systemic injection of lipopolysaccharide (LPS), and neurophysiological responses were recorded from the uncut chorda tympani 4-10 days after nerve section to determine if normal sodium sensitivity was restored. Rats receiving nerve section, dietary sodium restriction, and LPS exhibited normal sodium responses. In intact rats, injection of LPS alone or LPS injection combined with sodium restriction had no effect on taste responses to sodium stimuli. Surprisingly, combining nerve section, LPS injection, and maintenance of rats on a normal diet induced supersensitive responses to sodium. These findings are the first to demonstrate that the immune system can regulate peripheral gustatory function.

Sensitive periods for the effect of dietary sodium restriction on intact and denervated taste receptor cells

2002 ◽  
Vol 283 (5) ◽  
pp. R1275-R1284 ◽  
Author(s):  
Lynnette Phillips McCluskey ◽  
David L. Hill
Keyword(s):  
Taste Receptor ◽  
Taste Buds ◽  
Dietary Sodium ◽  
Chorda Tympani ◽  
Sodium Restriction ◽  
Chorda Tympani Nerve ◽  
Sensitive Periods ◽  
Low Sodium ◽  
Keratin 19 ◽  
Dietary Sodium Restriction

Unilateral chorda tympani nerve (CT) section combined with dietary sodium restriction leads to striking alterations in sodium taste function. The regenerated rat CT exhibits deficits in sodium sensitivity, and surprisingly, there are also functional alterations in the intact, contralateral nerve. The studies presented here describe the functional “sensitive periods” for these aberrations and the number of taste buds present during corresponding stages. The regenerated CT is sensitive to dietary sodium restriction during the first 2 wk after denervation, whereas the intact CT is sensitive to dietary manipulation during the first week postsection. Therefore, distinct mechanisms are responsible for the effects of sodium restriction combined with denervation, because separate sensitive periods exist for the regenerated and intact CT nerves. Identification of mature taste buds with an antibody directed at anti-keratin 19 revealed that there is a loss of ∼85% of taste buds on the denervated side of the tongue under control and low-sodium diets within the first week postsection. Thus, sodium restriction does not differentially affect the loss of taste buds following denervation.

Dietary sodium restriction exacerbates age-related changes in rat adipose tissue and liver lipogenesis

Metabolism ◽  
2003 ◽  
Vol 52 (8) ◽  
pp. 1072-1077 ◽  
Author(s):  
A.R Xavier ◽  
M.A.R Garófalo ◽  
R.H Migliorini ◽  
I.C Kettelhut
Keyword(s):  
Adipose Tissue ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Age Related ◽  
Dietary Sodium Restriction ◽  
Rat Adipose Tissue ◽  
Age Related Changes

scholarly journals The Effects of Short-Term Changes in Sodium Intake on Plasma Marinobufagenin Levels in Patients with Primary Salt-Sensitive and Salt-Insensitive Hypertension

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1502
Author(s):  
Katarzyna Łabno-Kirszniok ◽  
Agata Kujawa-Szewieczek ◽  
Andrzej Wiecek ◽  
Grzegorz Piecha
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Sodium Intake ◽  
Left Ventricular ◽  
Primary Hypertension ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Short Term ◽  
Salt Loading ◽  
Dietary Sodium Restriction

Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.

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