High dietary sodium enhances gustatory nerve activity and behavioral responses to NaCl

1991 ◽  
Vol 261 (1) ◽  
pp. R52-R58 ◽  
Author(s):  
T. W. Priehs ◽  
K. J. Mooney ◽  
R. A. Bernard
Keyword(s):  
Sodium Intake ◽  
Dietary Sodium ◽  
Apparent Difference ◽  
Chorda Tympani Nerve ◽  
High Salt Diet ◽  
Salt Diet ◽  
Stimulus Response ◽  
Electrophysiological Recordings ◽  
Gustatory Nerve ◽  
Preference Responses

Neural and behavioral taste responses to NaCl were studied in rats receiving a high-salt diet. Salt preferences and voluntary sodium intake were measured by the 24-h two-bottle choice method over a wide concentration range of NaCl solutions. As expected, the salt-loaded rats showed lower preference responses for all the solutions tested, which were presented in ascending order from 0.001 to 1.0 M NaCl. However, they freely ingested significantly greater amounts of sodium than the controls by drinking larger volumes of saline solution throughout the hypotonic concentration range, from 0.001 to 0.1 M NaCl. They showed lower voluntary intake of sodium only for isotonic and hypertonic solutions. Electrophysiological recordings from the chorda tympani nerve showed that the taste responses of the salt-loaded rats were greater in magnitude than those of the controls, and the neural stimulus-response function of the experimental group had a significantly steeper slope but no apparent difference in threshold. These experiments indicate that salt-loaded rats have enhanced appetitive responses to NaCl that may be mediated by increased sensory input.

scholarly journals P0166ADDITIVE INTERACTION OF HIGH SODIUM INTAKE AND INCREASED SERUM TRIGLYCERIDE ON HYPERTENSION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Joo-Hark Yi ◽  
Mi-yeon Yu ◽  
Jong Wook Choi ◽  
Sang-Woong Han ◽  
Chang Hwa Lee ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Interaction Analysis ◽  
Sodium Intake ◽  
Serum Triglyceride ◽  
Dietary Sodium ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Sodium ◽  
High Sodium Intake ◽  
Abnormal Lipid Metabolism

Abstract Background and Aims Both high salt diet and abnormal lipid metabolism are critical risks of vascular endothelial dysfunction. This study investigated the interactive effects of increased sodium intake and elevated serum triglyceride (TG) on elevated blood pressure (BP). Method We conducted nation-wide, population-based interaction analysis using Kawasaki method for estimating 24-h urinary sodium excretion (e24hUNaEKawasaki) as a candidate indicator of dietary sodium intake. Eligible as cases were all native Koreans aged 20 years or older without significant medical illness. Results: A total of 16936 participants were divided into quintiles according to their e24hUNaEKawasaki results. Participants in the highest quintile were more obese and hypertensive and had increased white blood cell count, decreased hemoglobin, greater glycemic exposure, and poor lipid profiles as compared to lower quintiles. Linear regression showed that e24UNaEKawasaki was closely related with dietary sodium intake, systolic BP, diastolic BP, and TG. Multiple logistic regression, adjusted for dietary sodium intake and various conventional risk factors of hypertension, demonstrated that both e24UNaEKawasaki and TG were significant predictors of hypertension. Our interaction analysis revealed that high sodium intake had a bigger effect on the risk of hypertension in participants with elevated TG than those without (adjusted RERI = 0.022, 95% CI = 0.017-0.027; adjusted AP = 0.017, 95% CI = 0.006-0.028; adjusted SI = 1.010, 95% CI = 1.007-1.014). Conclusion Our findings indicate that the interaction of high salt diet and abnormal lipid metabolism may exert synergistic biologic effect on the increased arterial BP.

Renal nerves and catecholamine excretion

1981 ◽  
Vol 240 (1) ◽  
pp. F75-F81 ◽  
Author(s):  
N. Morgunov ◽  
A. D. Baines
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Renal Nerves ◽  
High Salt Diet ◽  
Salt Diet ◽  
Catecholamine Excretion ◽  
Low Salt ◽  
Baroreceptor Stimulation ◽  
Chronic Denervation

To determine which neurotransmitters are released into urine by renal nerves, we either acutely denervated one kidney or stimulated renal nerves by activation of the baroreflex. Acute denervation increased dopamine (DA) and decreased norepinephrine (NE) excretion from the denervated kidney. In contrast, DA excretion decreased and NE excretion increased progressively from the contralateral innervated kidney. Sodium excretion related directly to DA and inversely to NE excretion. In chronic denervation experiments, baroreceptor stimulation increased NE excretion by 25% more from the innervated kidney than from its contralateral denervated mate, while DA excretion increased by 50% only from the innervated kidney. Baroreflex-stimulated NE and DA excretion from innervated kidneys was reduced by prior feeding of a low salt diet. The response was completely abolished by a high salt diet. Sodium excretion increased by the same proportion from innervated and chronically denervated kidneys following baroreceptor stimulation. In conclusion, 1) renal nerves release both NE and DA, 2) after acute unilateral denervation sodium excretion related directly with DA and inversely with NE excretion, and 3) urinary excretion of NE and DA derived from renal nerves was influenced by dietary sodium intake.

Renal endothelin in chronic angiotensin II hypertension

2002 ◽  
Vol 283 (1) ◽  
pp. R243-R248 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Jennifer S. Pollock ◽  
David M. Pollock
Keyword(s):  
Sodium Intake ◽  
Renal Tissue ◽  
High Salt ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Outer Medulla ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sprague Dawley Rats ◽  
Saline Vehicle

To determine the influence of chronic ANG II infusion on urinary, plasma, and renal tissue levels of immunoreactive endothelin (ET), ANG II (65 ng/min) or saline vehicle was delivered via osmotic minipump in male Sprague-Dawley rats given either a high-salt diet (10% NaCl) or normal-salt diet (0.8% NaCl). High-salt diet alone caused a slight but not statistically significant increase (7 ± 1%) in mean arterial pressure (MAP). MAP was significantly increased in ANG II-infused rats (41 ± 10%), and the increase in MAP was significantly greater in ANG II rats given a high-salt diet (59 ± 1%) compared with the increase observed in rats given a high-salt diet alone or ANG II infusion and normal-salt diet. After a 2-wk treatment, urinary excretion of immunoreactive ET was significantly increased by ∼50% in ANG II-infused animals and by over 250% in rats on high-salt diet, with or without ANG II infusion. ANG II infusion combined with high-salt diet significantly increased immunoreactive ET content in the cortex and outer medulla, but this effect was not observed in other groups. In contrast, high-salt diet, with or without ANG II infusion, significantly decreased immunoreactive ET content within the inner medulla. These data indicate that chronic elevations in ANG II levels and sodium intake differentially affect ET levels within the kidney and provide further support for the hypothesis that the hypertensive effects of ANG II may be due to interaction with the renal ET system.

Salt intake and insulin sensitivity in healthy human volunteers

2007 ◽  
Vol 113 (3) ◽  
pp. 141-148 ◽  
Author(s):  
Raymond R. Townsend ◽  
Shiv Kapoor ◽  
Christopher B. McFadden
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Infusion ◽  
Salt Intake ◽  
Sodium Intake ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Euglycaemic Clamp ◽  
Noradrenaline Concentration ◽  
Low Salt

The literature on salt intake and insulin sensitivity presents a mixed picture, as some studies have shown an increase, whereas others have shown a decrease, in insulin action as sodium intake is enhanced. In some cases, this may relate to the study of salt intake in patients with co-morbidities such as hypertension or diabetes. In the present study, we selected healthy normotensive lean volunteers who underwent a euglycaemic clamp following 6 days of a low-salt diet (20 mmol sodium daily) and, subsequently, 6 days of a high-salt diet (200 mmol sodium daily). Our results show an increase in insulin-mediated glucose disposal during euglycaemic clamp conditions that was significantly higher following the high-salt diet compared with the low-salt diet (7.41±0.41 compared with 6.11±0.40 mg·kg−1 of body weight·min−1 respectively; P=0.03). We measured calf blood flow before and during insulin infusion (no significant change after the two dietary salt interventions was detected) and plasma non-esterified fatty acids (also no significant differences were detected). We observed the expected increases in renin concentration and aldosterone activity in subjects on the low-salt diet, and also observed a significantly less increase in plasma noradrenaline concentration during euglycaemic insulin infusion following the high-salt compared with the low-salt diet. We propose that the 4–5-fold increase in serum aldosterone and the greater increase in plasma noradrenaline concentration following the low-salt intervention compared with the high-salt period may have contributed to the differences in insulin sensitivity following the adjustment in dietary sodium intake.

scholarly journals Studies of Salt and Stress Sensitivity on Arterial Pressure in Renin-b Deficient Mice

2021 ◽  
Author(s):  
Pablo Nakagawa ◽  
Javier Gomez ◽  
Ko-Ting Lu ◽  
Justin L. Grobe ◽  
Curt D. Sigmund
Keyword(s):  
Blood Pressure ◽  
Restraint Stress ◽  
Sodium Intake ◽  
High Salt ◽  
Ventrolateral Medulla ◽  
High Salt Diet ◽  
Blood Pressure Elevation ◽  
Salt Diet ◽  
The Brain ◽  
Deficient Mice

AbstractExcessive sodium intake is known to increase the risk for hypertension, heart disease, and stroke. Individuals who are more susceptible to the effects of high salt are at higher risk for cardiovascular diseases even independent of their blood pressure status. Local activation of the renin-angiotensin system (RAS) in the brain, among other mechanisms, has been hypothesized to play a key role in contributing to salt balance. We have previously shown that deletion of the alternative renin isoform termed renin-b disinhibits the classical renin-a encoding preprorenin in the brain resulting in elevated brain RAS activity. Thus, we hypothesized that renin-b deficiency results in higher susceptibility to salt-induced elevation in blood pressure. Telemetry implanted Ren-bNull and wildtype littermate mice were first offered a low salt diet for a week and subsequently a high salt diet for another week. A high salt diet induced a mild blood pressure elevation in both Ren-bNull and wildtype mice, but mice lacking renin-b did not exhibit an exaggerated pressor response. When renin-b deficient mice were exposed to a high salt diet for a longer duration (4 weeks), was a trend for increased myocardial enlargement in Ren-bNull mice when compared with control mice. Multiple studies have also demonstrated the association of chronic and acute environmental stress with hypertension. Activation of the RAS in the rostral ventrolateral medulla and the hypothalamus is required for stress-induced hypertension. Thus, we next questioned whether the lack of renin-b would result in exacerbated response to an acute restraint-stress. Wildtype and Ren-bNull mice equally exhibited elevated blood pressure in response to restraint-stress, which was similar in mice fed either a low or high salt diet. These studies highlight a complex mechanism that masks/unmasks roles for renin-b in cardiovascular physiology.

Renal endosomes contain angiotensin peptides, converting enzyme, and AT1A receptors

1999 ◽  
Vol 277 (2) ◽  
pp. F303-F311 ◽  
Author(s):  
John D. Imig ◽  
Gabriel L. Navar ◽  
Li-Xian Zou ◽  
Katie C. O’Reilly ◽  
Patricia L. Allen ◽  
...  
Keyword(s):  
High Salt ◽  
Dietary Sodium ◽  
Kidney Cortex ◽  
Ang Ii ◽  
Converting Enzyme ◽  
High Salt Diet ◽  
Salt Diet ◽  
Angiotensin Peptides ◽  
Low Salt ◽  
Ace Activity

Kidney cortex and proximal tubular angiotensin II (ANG II) levels are greater than can be explained on the basis of circulating ANG II, suggesting intrarenal compartmentalization of these peptides. One possible site of intracellular accumulation is the endosomes. In the present study, we tested for endosomal ANG I, ANG II, angiotensin type 1A receptor (AT1A), and angiotensin converting enzyme (ACE) activity and determined whether these levels are regulated by salt intake. Male Sprague-Dawley rats were fed chow containing either high or low dietary sodium for 10–14 days. Blood and kidneys were harvested and processed for measurement of plasma, kidney, and renal intermicrovillar cleft and endosomal angiotensin levels. Kidney ANG I averaged 179 ± 20 fmol/g and ANG II averaged 258 ± 36 fmol/g in rats fed a high-sodium diet and were significantly higher, averaging 347 ± 58 fmol/g and 386 ± 55 fmol/g, respectively, in rats fed a low-salt diet. Renal intermicrovillar clefts and endosomes contained ANG I and ANG II. Intermicrovillar cleft ANG I and ANG II levels averaged 8.4 ± 2.6 and 74 ± 26 fmol/mg, respectively, in rats fed a high-salt diet and 7.6 ± 1.7 and 70 ± 25 fmol/mg in rats fed a low-salt diet. Endosomal ANG I and ANG II levels averaged 12.3 ± 4.4 and 43 ± 19 fmol/mg, respectively, in rats fed a high-salt diet, and these levels were similar to those observed in rats fed a low-salt diet. Renal endosomes from rats fed a low-salt diet demonstrated significantly more AT1A receptor binding compared with rats fed a high-salt diet. ACE activity was detectable in renal intermicrovillar clefts and was 2.5-fold higher than the levels observed in renal endosomes. Acute enalaprilat treatment decreased ACE activity in renal intermicrovillar clefts by 90% and in renal endosomes by 84%. Likewise, intermicrovillar cleft and endosomal ANG II levels decreased by 61% and 52%, respectively, in enalaprilat-treated animals. These data demonstrate the presence of intact angiotensin peptides and ACE activity in renal intermicrovillar clefts and endosomes, indicating that intact angiotensin peptides are formed and/or trafficked through intracellular endosomal compartments and are dependent on ACE activity.

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.

scholarly journals Atrial natriuretic peptide and aldosterone secretions, and atrial natriuretic peptide-binding sites in kidneys and adrenal glands of pregnant and fetal rats in late gestation in response to a high-salt diet

2000 ◽  
pp. 524-532 ◽  
Author(s):  
S Deloof ◽  
C De Seze ◽  
V Montel ◽  
A Chatelain
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Adrenal Glands ◽  
Sodium Intake ◽  
High Salt ◽  
Pregnant Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Sodium ◽  
Fetal Rats

OBJECTIVE: This study aimed at determining, in the term pregnant rat, whether maternal and fetal plasma atrial natriuretic peptide (ANP) concentrations were modified in response to an oral sodium load, and to investigate whether any changes in plasma concentrations were able to modify the density and affinity of the different ANP-binding site subtypes in maternal and fetal kidneys and adrenal glands. METHODS: Pregnant rats kept in metabolic cages were divided into two groups. The normal sodium diet group had free access to rat chow and tap water whereas the high sodium diet group received 1% NaCl as drinking water for 10 consecutive days from day 11 to day 21 of gestation with free access to standard rat chow. Pregnant rats from both groups were killed by decapitation on day 21 of gestation. The plasma ANP and aldosterone concentrations were determined by RIA. The density and affinity of ANP receptors were determined in the maternal and fetal adrenal glands and kidneys. RESULTS: In the pregnant rats on the high-salt diet, the sodium and water intakes, as well as the urine volume and sodium excretion, were significantly higher than in the control group. After 10 days of high-salt intake, water and sodium retentions were not significantly different in the two groups, indicating that the pregnant rats were able to excrete excess salt. The high sodium intake did not change the body weight of the pregnant rats but did increase the body weight of the fetal rats. Maternal and fetal hematocrits remained unchanged in both groups, the high sodium intake did not modify plasma sodium concentration in the maternal rats but increased that of the fetuses, indicating an accumulation of sodium in the fetal rats. The dietary sodium intake did not change the plasma ANP concentrations but significantly decreased the plasma aldosterone concentrations in both the maternal and fetal rats. In response to the high-salt diet, the density and affinity of total ANP, ANPb and ANPc receptors were not altered in the maternal isolated renal glomeruli or the adrenal zona glomerulosa membranes or the fetal adrenal gland and kidney membrane preparations. CONCLUSION: These results suggest that ANP is not involved in the regulation of water and electrolyte balance in maternal and fetal rats during salt-loaded intake.

scholarly journals Renal medullary endothelin-1 is decreased in Dahl salt-sensitive rats

2011 ◽  
Vol 301 (2) ◽  
pp. R519-R523 ◽  
Author(s):  
Joshua S. Speed ◽  
Babbette LaMarca ◽  
Hunter Berry ◽  
Kathy Cockrell ◽  
Eric M. George ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Renal Medulla ◽  
Receptor Expression ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Sodium ◽  
Endothelin System ◽  
Chronic Infusion ◽  
Salt Sensitive Hypertension

Although it is well established that the renal endothelin (ET-1) system plays an important role in regulating sodium excretion and blood pressure through activation of renal medullary ETB receptors, the role of this system in Dahl salt-sensitive (DS) hypertension is unclear. The purpose of this study was to determine whether the DS rat has abnormalities in the renal medullary endothelin system when maintained on a high sodium intake. The data indicate that Dahl salt-resistant rats (DR) on a high-salt diet had a six-fold higher urinary endothelin excretion than in the DR rats with low Na+ intake (17.8 ± 4 pg/day vs. 112 ± 44 pg/day). In sharp contrast, urinary endothelin levels increased only twofold in DS rats in response to a high Na+ intake (13 ± 2 pg/day vs. 29.8 ± 5.5 pg/day). Medullary endothelin concentration in DS rats on a high-Na+ diet was also significantly lower than DR rats on a high-Na+ diet (31 ± 2.8 pg/mg vs. 70.9 ± 5 pg/mg). Furthermore, DS rats had a significant reduction in medullary ETB receptor expression compared with DR rats while on a high-Na+ diet. Finally, chronic infusion of ET-1 directly into the renal medulla blunted Dahl salt-sensitive hypertension. These data indicate that a decrease in medullary production of ET-1 in the DS rat could play an important role in the development of salt-sensitive hypertension observed in the DS rat.

Low environmental temperature modulates gustatory nerve activity and behavioral responses to NaCl in rats

1999 ◽  
Vol 277 (2) ◽  
pp. R368-R373 ◽  
Author(s):  
Yasutake Shimizu ◽  
Keiichi Tonosaki
Keyword(s):  
Ambient Temperature ◽  
Cold Exposure ◽  
Cell Function ◽  
Preference Test ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Sodium Channel Blocker ◽  
Behavioral Studies ◽  
Electrophysiological Recordings ◽  
Gustatory Nerve

We studied the effects of cold ambient temperature on chorda tympani nerve responses to taste stimuli such as sucrose, NaCl, quinine HCl (QHCl), and HCl in rats. The electrophysiological recordings of the whole chorda tympani nerves from control (22°C) and cold-exposed (4°C) rats revealed that the responses to sucrose, HCl, and QHCl were unaffected by cold exposure. In contrast, the nerve responses to NaCl were enhanced time dependently, reaching a maximum 7–14 days after cold exposure. Responses to sodium acetate were likewise elevated as they were to NaCl, whereas those to KCl were unchanged after cold exposure. In addition, the residual NaCl responses after lingual application of the sodium-channel blocker amiloride in cold-exposed rats were similar to those in control animals. It is thus most likely that cold exposure potentiates the chorda tympani nerve responses to Na+, but not to Cl−. Behavioral studies with the two-bottle preference test showed that the cold-exposed rats refused to drink NaCl solutions at 0.05 and 0.1 M, the concentrations being preferred by control animals. These results suggest that the ambient temperature influences taste cell function, and that the enhanced NaCl response of the chorda tympani nerve is related to the avoidance of NaCl intake under cold environment.

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