Commercial rodent diets contain more sodium than rats need

2005 ◽  
Vol 288 (2) ◽  
pp. F428-F431 ◽  
Author(s):  
Wesley Martus ◽  
Dennis Kim ◽  
Jeffrey L. Garvin ◽  
William H. Beierwaltes
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Caloric Intake ◽  
Sodium Content ◽  
Dietary Sodium ◽  
Renal Physiology ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Pelleted Diet ◽  
Experimental Group

The dietary sodium requirements for rats have been a matter of debate. Our hypothesis was that normal commercial rodent chow contains sodium in excess of dietary needs and that this could have a significant impact on cardiovascular and renal physiology. To investigate dietary sodium requirements, 3-wk-old weanling Sprague-Dawley rats were fed a custom pelleted diet containing no sodium that was isocaloric to normal commercial rodent chow. These rats were provided with two drinking bottles; one contained water, and the other contained 0.5% NaCl. Thus they could choose and consume sodium as needed. Age-matched controls received normal pelleted Harlan Teklad 22/5 rodent diet (0.5% sodium content) and water ad libitum. Body weight and liquid intake were monitored over 7 wk until the rats were 10 wk old. At the end of the study, blood pressure was recorded. Weekly sodium intake in the experimental group was only 15% of that reported for rats fed normal rodent chow beginning in the first week postweaning. Growth was identical in the two groups (7.8 ± 0.1 vs. 7.6 ± 0.1 g/day), as was the total fluid volume intake. Blood pressure was significantly lower in the experimental rats compared with controls (96 ± 4 vs. 122 ± 4 mmHg, P < 0.05). These data suggest that, when given the choice, rats will consume significantly less sodium than provided in commercial chow, without any alteration in their growth rate. Rats fed standard commercial rodent chow may consume at least seven times more sodium than is necessary. This suggests commercial rodent diets may force excess sodium to accommodate caloric intake.

scholarly journals Norepinephrine-evoked salt-sensitive hypertension requires impaired renal sodium chloride cotransporter activity in Sprague-Dawley rats

2016 ◽  
Vol 310 (2) ◽  
pp. R115-R124 ◽  
Author(s):  
Kathryn R. Walsh ◽  
Jill T. Kuwabara ◽  
Joon W. Shim ◽  
Richard D. Wainford
Keyword(s):  
Blood Pressure ◽  
Sodium Chloride ◽  
Salt Sensitivity ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sodium Chloride Cotransporter ◽  
Sprague Dawley Rats ◽  
Salt Sensitive Hypertension ◽  
The Impact

Recent studies have implicated a role of norepinephrine (NE) in the activation of the sodium chloride cotransporter (NCC) to drive the development of salt-sensitive hypertension. However, the interaction between NE and increased salt intake on blood pressure remains to be fully elucidated. This study examined the impact of a continuous NE infusion on sodium homeostasis and blood pressure in conscious Sprague-Dawley rats challenged with a normal (NS; 0.6% NaCl) or high-salt (HS; 8% NaCl) diet for 14 days. Naïve and saline-infused Sprague-Dawley rats remained normotensive when placed on HS and exhibited dietary sodium-evoked suppression of peak natriuresis to hydrochlorothiazide. NE infusion resulted in the development of hypertension, which was exacerbated by HS, demonstrating the development of the salt sensitivity of blood pressure [MAP (mmHg) NE+NS: 151 ± 3 vs. NE+HS: 172 ± 4; P < 0.05]. In these salt-sensitive animals, increased NE prevented dietary sodium-evoked suppression of peak natriuresis to hydrochlorothiazide, suggesting impaired NCC activity contributes to the development of salt sensitivity [peak natriuresis to hydrochlorothiazide (μeq/min) Naïve+NS: 9.4 ± 0.2 vs. Naïve+HS: 7 ± 0.1; P < 0.05; NE+NS: 11.1 ± 1.1; NE+HS: 10.8 ± 0.4). NE infusion did not alter NCC expression in animals maintained on NS; however, dietary sodium-evoked suppression of NCC expression was prevented in animals challenged with NE. Chronic NCC antagonism abolished the salt-sensitive component of NE-mediated hypertension, while chronic ANG II type 1 receptor antagonism significantly attenuated NE-evoked hypertension without restoring NCC function. These data demonstrate that increased levels of NE prevent dietary sodium-evoked suppression of the NCC, via an ANG II-independent mechanism, to stimulate the development of salt-sensitive hypertension.

scholarly journals Chronic high-sodium intake elevates blood pressure and reduces bone mass in male Sprague-Dawley rats

Bone Reports ◽  
2020 ◽  
Vol 13 ◽  
pp. 100519
Author(s):  
Wacharaporn Tiyasatkulkovit ◽  
Siriorn Aksornthong ◽  
Kanikar Wongdee ◽  
Nattapon Panupinthu ◽  
Narattaphol Charoenphandhu
Keyword(s):  
Blood Pressure ◽  
Bone Mass ◽  
Sodium Intake ◽  
Sprague Dawley ◽  
High Sodium ◽  
High Sodium Intake ◽  
Sprague Dawley Rats

Conscious obese rats have impaired reflex bradycardia and enhanced norepinephrine sensitivity

1996 ◽  
Vol 271 (3) ◽  
pp. R654-R660 ◽  
Author(s):  
R. D. Bunag ◽  
M. Meyer ◽  
N. Vansell ◽  
L. Kerecsen
Keyword(s):  
Blood Pressure ◽  
Serum Insulin ◽  
Caloric Intake ◽  
Subsequent Development ◽  
Systemic Arterial Pressure ◽  
Sprague Dawley ◽  
Reflex Bradycardia ◽  
Sprague Dawley Rats ◽  
Reflex Tachycardia ◽  
Basal Blood Pressure

Male Sprague-Dawley rats fed a condensed milk diet were classified as either "obesity susceptible" (OS) or "obesity resistant" (OR) based on body weight increases attained after 12 wk. Overall caloric intake in OS rats was higher than in chow-fed controls, and OS rats were heavier than chow-fed controls or OR rats. There were no significant differences in blood glucose, serum insulin, ventricular weight, basal blood pressure, or heart rate. Pressor responses recorded after combined blockade with atropine and propranolol to eliminate reflex effects were identical for vasopressin, but those to norepinephrine were larger in OS than in OR rats, whereas those to angiotensin were larger in OS than in control rats. When baroreflex sensitivity was assessed using intravenously infused sodium nitroprusside or phenylephrine to alter systemic arterial pressure, differences in reflex tachycardia were equivocal, but reflex bradycardia was clearly inhibited in OS rats. These results show that, although basal blood pressure was unaffected in OS rats, their impaired reflex bradycardia along with enhanced pressor responsiveness to norepinephrine could predispose them to subsequent development of hypertension.

Role of endogenous central opioid mechanisms in maintenance of body sodium balance

1995 ◽  
Vol 268 (3) ◽  
pp. R723-R730 ◽  
Author(s):  
D. R. Kapusta ◽  
J. C. Obih
Keyword(s):  
Sodium Intake ◽  
Dietary Sodium ◽  
Opioid Antagonist ◽  
Sodium Balance ◽  
Sodium Restriction ◽  
Sprague Dawley ◽  
Intracerebroventricular Infusion ◽  
Sprague Dawley Rats ◽  
Body Sodium

The role of endogenous central opioids in the regulation of renal function was studied in Sprague-Dawley rats. In metabolism studies, changes in sodium balance were examined during normal dietary sodium intake (days 1-7; Na+ of 174 meq/kg) and sodium restriction (days 8-14; Na+ of 4.0 meq/kg). The influence of endogenous central opioids was investigated by repeating the protocol in the same rats during intracerebroventricular infusion of the opioid antagonist naltrexone methylbromide (NMBR). Intracerebroventricular NMBR did not alter sodium balance in rats fed normal sodium chow. In contrast, on low-sodium days 8 and 9, rats exhibited a more negative sodium balance during intracerebroventricular NMBR (day 8; -1,191 +/- 37 mu eq) compared with respective predrug control levels (day 8; -641 +/- 39 mu eq). Subcutaneous NMBR did not alter renal adaptation to sodium restriction. Thus central opioids are not involved in the maintenance of sodium balance during normal sodium intake. However, when dietary sodium is restricted, central opioid pathways are activated as a mechanism to maximally retain sodium.

scholarly journals Sodium Content of Processed Meats in New Zealand

Proceedings ◽  
2019 ◽  
Vol 37 (1) ◽  
pp. 42
Author(s):  
Borderon ◽  
Eyles ◽  
Mhurchu ◽  
Young ◽  
Bradbury
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
New Zealand ◽  
Sodium Intake ◽  
Sodium Content ◽  
Major Risk Factor ◽  
Dietary Sodium ◽  
Processed Meats

High dietary sodium intake increases blood pressure, a major risk factor for cardiovascular disease. [...]

scholarly journals The role of caloric intake in the association of high salt intake with high blood pressure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Naftali Stern ◽  
Assaf Buch ◽  
Rebecca Goldsmith ◽  
Lesley Nitsan ◽  
Miri Margaliot ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Substantial Reduction ◽  
Caloric Intake ◽  
Community Dwelling ◽  
Dietary Sodium ◽  
Cross Sectional Survey ◽  
High Salt Intake

AbstractSince current recommendations call for a substantial reduction in overall sodium consumption, we tested whether or not these recommendations are implemented in common large subpopulations such as those with abnormal weight or hypertension in the current high sodium, high-calorie nutritional environment. In a national representative cross-sectional survey of the community-dwelling subjects aged 25–65 years conducted in Israel between 2015 and 2017, 582 randomly selected subjects completed health and dietary questionnaires, underwent blood pressure and anthropometric measurements and collected 24-h urine specimens, to assess dietary sodium intake. Overall mean 24-h sodium excretion was 3834 mg, more than double the recommended upper intake for adults < 1500 mg/day. Sodium excretion was directly related to caloric intake and blood pressure and linked to the presence of hypertension and overweight/obesity. The highest sodium excretion was seen in overweight/obese hypertensive subjects. This recent national survey shows a high consumption of sodium in the Israeli population and a dose–response association between caloric intake and urinary sodium excretion, independent of BMI and hypertension. Nevertheless, overweight/obese subjects with hypertension consume (excrete) more sodium than other BMI/ blood pressure-related phenotypes and may thus comprise a target subpopulation for future efforts to reduce sodium intake.

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)

scholarly journals Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. R1546-R1554 ◽  
Author(s):  
Melissa Li ◽  
Xiaoling Dai ◽  
Stephanie Watts ◽  
David Kreulen ◽  
Gregory Fink
Keyword(s):  
Blood Pressure ◽  
Sympathetic Innervation ◽  
Sympathetic Ganglia ◽  
Plasma Norepinephrine ◽  
Sprague Dawley ◽  
Surgical Ablation ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Hypertension Development

Endothelin (ET) type B receptors (ETBR) are expressed in multiple tissues and perform different functions depending on their location. ETBR mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ETBR in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.

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.

Blood Pressure and Intra-Erythrocyte Sodium during Normal and High Salt Intake in Middle-Aged Men: Relationship to Family History of Hypertension, and Neurogenic and Hormonal Variables

1984 ◽  
Vol 66 (4) ◽  
pp. 427-433 ◽  
Author(s):  
Ottar Gudmundsson ◽  
Hans Herlitz ◽  
Olof Jonsson ◽  
Thomas Hedner ◽  
Ove Andersson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Family History ◽  
Salt Intake ◽  
Sodium Intake ◽  
Positive Family History ◽  
Sodium Content ◽  
High Salt Intake ◽  
History Of ◽  
Family History Of Hypertension ◽  
Erythrocyte Sodium

1. During 4 weeks 37 normotensive 50-year-old men identified by screening in a random population sample were given 12 g of NaCl daily, in addition to their usual dietary sodium intake. Blood pressure, heart rate, weight, urinary excretion of sodium, potassium and catecholamines, plasma aldosterone and noradrenaline and intra-erythrocyte sodium content were determined on normal and increased salt intake. The subjects were divided into those with a positive family history of hypertension (n = 11) and those without such a history (n = 26). 2. Systolic blood pressure and weight increased significantly irrespective of a positive family history of hypertension. 3. On normal salt intake intra-erythrocyte sodium content was significantly higher in those with a positive family history of hypertension. During high salt intake intra-erythrocyte sodium content decreased significantly in that group and the difference between the hereditary subgroups was no longer significant. 4. In the whole group urinary excretion of noradrenaline, adrenaline and dopamine increased whereas plasma aldosterone decreased during the increased salt intake. 5. Thus, in contrast to some earlier studies performed in young subjects, our results indicate that moderately increased sodium intake acts as a pressor agent in normotensive middle-aged men whether there was a positive family history of hypertension or not. We confirm that men with positive family history of hypertension have an increased intra-erythrocyte sodium content, and that an increase in salt intake seems to increase overall sympathetic activity.

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