Salt Loading in Canola Oil Fed SHRSP Rats Induces Endothelial Dysfunction

Papazzo, Annateresa; Conlan, Xavier A.; Lexis, Louise; Charchar, Fadi J.; Lewandowski, Paul

doi:10.1371/journal.pone.0066655

Cited by 7 publications

(10 citation statements)

References 39 publications

(63 reference statements)

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“…The SHRSP is characterized by even higher BPs than SHR, a tendency to die from stroke, and a sensitivity to salt. The SHRSP presents with an increase in oxidative stress, a reduction in nitric oxide availability, and endothelial dysfunction [12, 13, 21, 25]. A decrease in nitric oxide bioavailability has been previously shown to induce strong aortic stiffening [17, 26].…”

Section: Discussionmentioning

confidence: 99%

“…The reasons for this are multifactorial, including endothelial [13] and renal dysfunction [14]. Since the endothelium is a primary means of maintaining vascular smooth muscle integrity [15] and renal dysfunction is associated with arterial stiffness [16], it was hypothesized that this model was relevant for analyzing arterial remodeling associated with stiffness.…”

Section: Introductionmentioning

confidence: 99%

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Differential Stiffening between the Abdominal and Thoracic Aorta: Effect of Salt Loading in Stroke-Prone Hypertensive Rats

et al. 2018

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Central artery stiffening is recognized as a cardiovascular risk. The effects of hypertension and aging have been shown in human and animal models but the effect of salt is still controversial. We studied the effect of a high-salt diet on aortic stiffness in salt-sensitive spontaneously hypersensitive stroke-prone rats (SHRSP). Distensibility, distension, and β-stiffness were measured at thoracic and abdominal aortic sites in the same rats, using echotracking recording of the aortic diameter coupled with blood pressure (BP), in SHRSP-salt (5% salted diet, 5 weeks), SHRSP, and normotensive Wistar-Kyoto (WKY) rats. Hemodynamic parameters were measured at BP matched to that of WKY. Histological staining and immunohistochemistry were used for structural analysis. Hemodynamic isobaric parameters in SHRSP did not differ from WKY and only those from the abdominal aorta of SHRSP-salt presented decreased distensibility and increased stiffness compared with WKY and SHRSP. The abdominal and thoracic aortas presented similar thickening, increased fibrosis, and remodeling with no change in collagen content. SHRSP-salt presented a specific increased elastin disarray at the abdominal aorta level but a decrease in elastin content in the thoracic aorta. This study demonstrates the pro-stiffening effect of salt in addition to hypertension; it shows that only the abdominal aorta presents a specific pressure-independent stiffening, in which elastin disarray is likely a key mechanism.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Differential Stiffening between the Abdominal and Thoracic Aorta: Effect of Salt Loading in Stroke-Prone Hypertensive Rats

et al. 2018

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“…In addition to the survival test, another animal experiment was conducted to further investigate the effects of full hydrogenation on blood pressure, lipid levels in serum, and histological analyses. In this experiment, the Soy diet was used as a negative control, as in previous studies [ 14 – 18 , 33 ]. Notably, Soy is the main fat source of CE-2, and no significant difference was found in survival times of SHRSP fed a 10 % Soy diet and original CE-2 (unpublished data).…”

Section: Methodsmentioning

confidence: 99%

“…Hence, the determinative substance for lifespan shortening remains unknown. In addition to the lifespan shortening, Can in SHRSP causes renal dysfunction [ 12 ], decreases blood cell membrane deformability [ 7 ], increases blood pressure, inhibits the Na + /K + –ATPase function [ 13 ], suppresses the reproductive activity [ 14 ], perturbs steroidal hormone levels [ 15 ], and increases oxidative stress [ 16 – 18 ]. Furthermore, these effects of Can have been reported in rats of other strains and in other animal species [ 19 – 23 ].…”

Section: Introductionmentioning

confidence: 99%

Fully hydrogenated canola oil extends lifespan in stroke-prone spontaneously hypertensive rats

et al. 2021

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Background Canola oil (Can) and several vegetable oils shorten the lifespan of stroke-prone spontaneously hypertensive rats (SHRSP). Although similar lifespan shortening has been reported for partially hydrogenated Can, the efficacy of fully hydrogenated oils on the lifespan remains unknown. The present study aimed to investigate the lifespan of SHRSP fed diets containing 10 % (w/w) of fully hydrogenated Can (FHCO) or other oils. Methods Survival test: Upon weaning, male SHRSP were fed a basal diet for rodents mixed with one of the test oils —i.e., FHCO, Can, lard (Lrd), and palm oil (Plm) throughout the experiment. The animals could freely access the diet and drinking water (water containing 1 % NaCl), and their body weight, food intake, and lifespan were recorded. Biochemical analysis test: Male SHRSP were fed a test diet with either FHCO, Can, or soybean oil (Soy) under the same condition, except to emphasize effects of fat, that no NaCl loading was applied. Soy was used as a fat source in the basal diet and was set the control group. Blood pressures was checked every 2 weeks, and serum fat levels and histological analyses of the brain and kidney were examined after 7 or 12 weeks of feeding. Results During the survival study period, the food consumption of FHCO-fed rats significantly increased (15–20 % w/w) compared with that of rats fed any other oil. However, the body weight gain in the FHCO group was significantly less (10–12 %) than that in the control group at 9–11 weeks old. The FHCO (> 180 days) intervention had the greatest effect on lifespan, followed by the Lrd (115 ± 6 days), Plm (101 ± 2 days), and Can (94 ± 3 days) diets. FHCO remarkably decreased the serum cholesterol level compared with Can and the systolic blood pressure from 12 to 16 weeks of age. In addition, while some rats in the Can group exhibited brain hemorrhaging and renal dysfunction at 16 weeks old, no symptoms were observed in the FHCO group. Conclusion This current study suggests that complete hydrogenation decreases the toxicity of Can and even prolongs the lifespan in SHRSP.

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“…These rats are also an important model for studying attention deficit hyperactivity disorder (20)(21)(22)(23), and Alzheimer's related vascular pathology (24,25) in humans. The SHRSP rats exhibit multiple dysfunctions such as saltsensitive spontaneous hypertension, cortical lesions with a high incidence of stroke by ;16 wk of age, nephropathy, hyperactivity of the renin-angiotensin system, insulin resistance, and hypertriglyceridemia (17,(26)(27)(28)(29)(30). However, this model remains poorly characterized in terms of energy balance and its predisposition to developing obesity.…”

mentioning

confidence: 99%

Host genetics and diet composition interact to modulate gut microbiota and predisposition to metabolic syndrome in spontaneously hypertensive stroke‐prone rats

et al. 2019

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Metabolic syndrome encompasses obesity, glucose intolerance, hypertension, and dyslipidemia; however, the interactions between diet and host physiology that predispose to metabolic syndrome are incompletely understood. Here, we explored the effects of a high‐fat diet (HFD) on energy balance, gut microbiota, and risk factors of metabolic syndrome in spontaneously hypertensive stroke‐prone (SHRSP) and Wistar‐Kyoto (WKY) rats. We found that the SHRSP rats were hypertensive, hyperphagic, less sensitive to hypophagic effects of exendin‐4, and expended more energy with diminished sensitivity to sympathetic blockade compared to WKY rats. Notably, key thermogenic markers in brown and retroperitoneal adipose tissues and skeletal muscle were up‐regulated in SHRSP than WKY rats. Although HFD promoted weight gain, adiposity, glucose intolerance, hypertriglyceridemia, hepatic lipidosis, and hyperleptinemia in both SHRSP and WKY rats, the SHRSP rats weighed less but had comparable percent adiposity to WKY rats, which supports the use of HFD‐fed SHRSP rats as a unique model for studying the metabolically obese normal weight (MONW) phenotype in humans. Despite distinct strain differences in gut microbiota composition, diet had a preponderant impact on gut flora with some of the taxa being strongly associated with key metabolic parameters. Together, we provide evidence that interactions between host genetics and diet modulate gut microbiota and predispose SHRSP rats to develop metabolic syndrome.—Singh, A., Zapata, R. C., Pezeshki, A., Workentine, M. L., Chelikani, P. K. Host genetics and diet composition interact to modulate gut microbiota and predisposition to metabolic syndrome in spontaneously hypertensive stroke‐prone rats. FASEB J. 33, 6748–6766 (2019). http://www.fasebj.org

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Salt Loading in Canola Oil Fed SHRSP Rats Induces Endothelial Dysfunction

Cited by 7 publications

References 39 publications

Differential Stiffening between the Abdominal and Thoracic Aorta: Effect of Salt Loading in Stroke-Prone Hypertensive Rats

Differential Stiffening between the Abdominal and Thoracic Aorta: Effect of Salt Loading in Stroke-Prone Hypertensive Rats

Fully hydrogenated canola oil extends lifespan in stroke-prone spontaneously hypertensive rats

Host genetics and diet composition interact to modulate gut microbiota and predisposition to metabolic syndrome in spontaneously hypertensive stroke‐prone rats

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