Gut dysbiosis contributes to high fructose–induced salt-sensitive hypertension in Sprague-Dawley rats

Nutrition ◽  
2020 ◽  
Vol 75-76 ◽  
pp. 110766 ◽  
Author(s):  
Yang Chen ◽  
Yeyan Zhu ◽  
Chunying Wu ◽  
Aihua Lu ◽  
Mokan Deng ◽  
...  
Keyword(s):  
Sprague Dawley ◽  
Gut Dysbiosis ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Salt Sensitive Hypertension

Corrigendum to

Nutrition ◽  
2020 ◽  
Vol 77 ◽  
pp. 110845
Author(s):  
Yang Chen ◽  
Yeyan Zhu ◽  
Chunying Wu ◽  
Aihua Lu ◽  
Mokan Deng ◽  
...  
Keyword(s):  
Sprague Dawley ◽  
Gut Dysbiosis ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Salt Sensitive Hypertension

Abstract 41: Fructose Stimulates Na/H Exchanger 3 Activity and Enhances the Ability of Angiotensin II to Activate Na/H Exchanger 3 in the Proximal Tubule

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Pablo Cabral ◽  
Nancy Hong ◽  
Jeffrey Garvin
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Physiological Saline ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Basal Rate ◽  
Low Concentrations ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Salt Sensitive Hypertension

Consumption of high-fructose corn syrup as a sweetener has increased dramatically. Fructose has been implicated in the epidemic of diabetes, obesity and hypertension including salt-sensitive hypertension. However, the mechanisms are poorly understood. The proximal nephron reabsorbs 60-70% of the fluid and Na, and most of the filtered bicarbonate via Na/H exchanger 3. Enhanced proximal nephron transport has been implicated in several forms of hypertension. We hypothesized that fructose stimulates NHE3 activity and enhances the ability of angiotensin II (ANG II) to activate NHE3 in the proximal tubule. To test our hypothesis we isolated and perfused proximal tubules from Sprague Dawley rats. NHE3 activity was measured as the recovery of intracellular pH after an NH4Cl acid pulse using the pH sensitive dye BCECF. The rate of pH recovery was measured in Fluorescent Units per second (FU/sec). In the presence of a 5.5 mM glucose-containing physiological saline the basal rate of pH recovery was 3.1 ± 0.8 FU/sec. When the luminal solution was exchanged to a 0.6 mM glucose + 5 mM fructose-containing physiological saline in a second period, the rate of pH recovery increased to 5 ± 1 FU/sec (p<0.03, n=8).To study whether this effect was due to the addition of fructose or the removal of glucose to the lumen, we performed a separate set of experiments where 5 mM glucose was substituted for 5 mM fructose. In the presence of 0.6 mM glucose the basal rate of pH recovery was 3.6 ± 1.5 FU/sec. When 5 mM fructose was added the rate of pH recovery increased to 5.9 ± 2 FU/sec (p<0.02, n=5). Control experiments showed no differences between periods when 5 mm glucose was added back to the luminal perfusate. Finally, we tested the effect of low concentrations of ANG II in the presence or absence of luminal fructose. In the presence of 5.5 mM glucose, ANG II 10-12 M did not affect the rate of pH recovery (change: -1.1 ± 0.5 FU/sec, n=9). However, in the presence of 5 mM fructose, ANG II increased the rate of pH recovery (change: 4.0 ± 2.2 FU/sec, p< 0.03 n=6). We conclude that acute treatment with fructose stimulates NHE3 activity and enhances the ability of ANG II to activate NHE3 in the proximal tubule. These results may partially explain the mechanism by which a fructose diet induces hypertension.

Abstract 328: High Fructose but not High Glucose Intake Induces Salt-sensitive Hypertension and Enhances NKCC2 Phosphorylation in Normal Rats.

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Emily Henson ◽  
Gustavo Ares ◽  
Mohammed Haque ◽  
Pablo Ortiz
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Salt Intake ◽  
High Salt ◽  
Sprague Dawley ◽  
High Fructose Diet ◽  
Fructose Intake ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Salt Sensitive Hypertension

Consumption of fructose as a sweetener has increased in the past three decades. A high-fructose diet has been implicated in the epidemic of diabetes, obesity, and hypertension. A third of the US population consumes 20-40% of their caloric intake from added sugars, with half of those calories from fructose. Little is known about the role of high fructose intake in renal salt handling and blood pressure regulation during high salt intake. In genetic models of salt-sensitive hypertension, the Na/K/2Cl cotransporter NKCC2 plays an important role by reabsorbing NaCl in the thick ascending limb (TAL). We hypothesized that 20% fructose in drinking water stimulates NKCC2 and sensitizes normal rats to high salt induced hypertension. Adult Sprague-Dawley rats were given 20% fructose or 20% glucose in drinking water for 1 week after which a high salt diet (4% Na in chow) was started. Systolic blood pressure (SBP) was measured every other day by tail cuff after 2 weeks of training. After one week of fructose or glucose alone, SBP did not change. In rats fed fructose, adding a 4% NaCl diet increased SBP to 128±6 mmHg by day 2 (p<0.01 vs glucose) and continued to increase up to 144±18 mmHg after 2 weeks on high salt (p<0.01 vs baseline; p<0.01 vs glucose). In glucose-fed rats high salt did not increase SBP (from 122±6 to 116±9 mmHg). 20% fructose alone for 3 weeks, or high salt alone did not change SBP. NKCC2 phosphorylation at Thr96,101 is associated with enhanced TAL NaCl reabsorption. We found that NKCC2 phosphorylation at Thr96,101 (normalized to total NKCC2) was higher in TALs isolated from rats fed fructose plus salt for 2 weeks compared to high salt alone (high-salt: 100%; fructose + high-salt: 250±40%, p<0.05). We concluded that a high fructose but not high glucose diet induces salt-sensitive hypertension in Sprague Dawley rats. This effect occurs within 1 week of a high fructose diet. In addition, a high fructose diet may stimulate NKCC2 activity by enhancing its phosphorylation. These data suggest that high fructose intake may increase blood pressure by preventing appropriate renal NaCl excretion during high dietary salt intake.

scholarly journals High-Fat-High-Fructose Diet Decreases Hippocampal Neuron Number in Male Rats

2020 ◽  
Vol 12 (1) ◽  
pp. 1-7
Author(s):  
Inggita Kusumastuty ◽  
Frinny Sembiring ◽  
Sri Andarini ◽  
Dian Handayani
Keyword(s):  
Cell Death ◽  
Nerve Cell ◽  
Hippocampal Neurons ◽  
Sprague Dawley ◽  
High Fat ◽  
Group I ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Group Ii ◽  
Nerve Cell Death

BACKGROUND: Consumption of foods and drinks high in energy, fat, and/or sugar beyond the recommended quantities can cause obesity, which triggers the incidence of brain nerve cell death related to oxidative stress, high levels of tumor necrosis factor (TNF)-α and triglycerides, and low high-density lipoprotein (HDL) levels. Progressive nerve cell death causes decreasing cognitive performance. This study aims to prove that an American Institute of Nutrition committee in 1993 (AIN-93M) diet modified with high-fat-high-fructose (HFHF) can decrease the number of hippocampal neurons. A decrease in the number of hippocampal neurons indicates progressive nerve cell death.METHODS: An experimental study using a post-test control group design was carried out using male Sprague Dawley rats. Samples were selected using simple random sampling to divide them into two groups, Group I was AIN-93M-modified HFHF diet (n=14) and Group II was AIN-93M standard (n=16). The number of visible neurons was measured in the hippocampus area of Sprague Dawley rats’ brains, stained with haemotoxylin and eosin (H&E) and scanned under 400x magnification. Neurons were counted in 10 visual fields using the "Cell_Count" application.RESULTS: The data were analysed by Pearson’s correlation test using SPSS. The results show that rats in Group I had a greater weight gain and fewer neurons than those in the Group II (p=0.023, r=-0.413).CONCLUSION: The consumption of foods high in fat and fructose can cause an increase in nerve cell death, as shown by the decrease in the number of hippocampal neurons.KEYWORDS: brain nerve cells, high fat, high fructose, increased body weight

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 Uric acid and glucose level in high fructose high cholesterol induced Sprague-Dawley rats after therapy with Acalypha indica Linn. ethanol extract

2019 ◽  
Author(s):  
Desak Gede Budi Krisnamurti ◽  
Fira Alyssa Gabriella Sinuraya ◽  
Tamara Ey Firsty ◽  
Rani Wardani Hakim ◽  
Erni H. Purwaningsih
Keyword(s):  
Uric Acid ◽  
Glucose Level ◽  
Ethanol Extract ◽  
Sprague Dawley ◽  
High Cholesterol ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Acalypha Indica

Antihypertensive effect of dietary calcium loading in angiotensin II-salt rats

1991 ◽  
Vol 261 (5) ◽  
pp. R1070-R1074 ◽  
Author(s):  
K. Ando ◽  
Y. Sato ◽  
A. Ono ◽  
K. Takahashi ◽  
T. Shimosawa ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Antihypertensive Effect ◽  
Hypotensive Effect ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Calcium Loading ◽  
Sprague Dawley Rats ◽  
Salt Sensitive Hypertension ◽  
Do So

To clarify the hypotensive effect of high dietary Ca intake on salt-sensitive hypertension, 7-wk-old Sprague-Dawley rats, 3.15% Na and/or 4.07% Ca diet loaded, were administered 125 ng/ml of angiotensin II (ANG II) intraperitoneally for 12 days. Compared with control rats (mean blood pressure 108 +/- 2 mmHg), ANG II administration caused hypertension (131 +/- 4 mmHg, P less than 0.05). Na loading enhanced the hypertensive effect of ANG II (161 +/- 4 mmHg, P less than 0.01). Dietary Ca loading did not significantly inhibit the pressor effect of ANG II alone (119 +/- 4 mmHg). However, Ca loading suppressed hypertension in ANG II-salt rats (126 +/- 4 mmHg, P less than 0.01). Plasma total catecholamine (norepinephrine + epinephrine) was increased in ANG II-salt rats (176 +/- 14 vs. 290 +/- 23 pg/ml, P less than 0.05), but Ca loading decreased plasma catecholamine (182 +/- 13 pg/ml, P less than 0.05). In contrast, plasma catecholamine was not significantly different between ANG II-treated rats with and without Ca loading. Ca loading increased serum Ca in ANG II rats (10.9 +/- 0.1 vs. 11.7 +/- 0.1 mg/dl, P less than 0.05) but did not do so significantly in ANG II-salt rats (10.8 +/- 0.2 vs. 10.9 +/- 0.1 mg/dl). Thus Ca loading exclusively ameliorated salt-sensitive hypertension, which was induced with ANG II administration and Na loading in rats, probably through suppression of the increased sympathetic activity. In addition, these effects of Ca loading were not mediated through an increased blood level of Ca.

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