Inhibition of endothelial nitric oxide synthase reverses the effect of exercise on improving cognitive function in hypertensive rats

Zhang, Liying; Zheng, Huiru; Luo, Jing; Li, Lili; Pan, Xiaona; Jiang, Ting; Xiao, Chen; Pei, Zhong; Hu, Xiquan

doi:10.1038/s41440-018-0033-5

Cited by 14 publications

(14 citation statements)

References 36 publications

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“…As the most commonly used animal models, data collection on rats and mice benefit from their short gestation periods and numerous off-spring. A number of modalities of exercise training such as treadmill running, voluntary wheel running, and swim training have been utilized on rat and mice models of various genetic backgrounds [9,45–48].…”

Section: Principle Of Animal Exercise Training Protocols and Sample Cmentioning

confidence: 99%

“…Several animal models and human epidemiological studies support the cardio-protective effect of exercise [4–6]. Several protective mechanisms demonstrated that exercise increased VO 2max (maximal oxygen consumption), improved cardiorespiratory fitness (CRF) [7], lipid profile [8], endothelial function [9], increased number of capillaries [10], and mitochondria anti-oxidant activity in the cardiovascular system [11]. However, while exercise typically results if beneficial effects on heart function, there are occasions when it could result in unexpected death during exercise especially for the CVD cohort [12–14].…”

Section: Introductionmentioning

confidence: 99%

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A systematic comparison of exercise training protocols on animal models of cardiovascular capacity

Feng

Wang

et al. 2019

Life Sciences

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Cardiovascular disease (CVD) is a major global cause of mortality, which has prompted numerous studies seeking to reduce the risk of heart failure and sudden cardiac death. While regular physical activity is known to improve CVD associated morbidity and mortality, the optimal duration, frequency, and intensity of exercise remains unclear. To address this uncertainty, various animal models have been used to study the cardioprotective effects of exercise and related molecular mechanism such as the mice training models significantly decrease size of myocardial infarct by affecting Kir6.1, VSMC sarc-KATP channels, and pulmonary eNOS. Although these findings cement the importance of animal models in studying exercise induced cardioprotection, the vast assortment of exercise protocols makes comparison across studies difficult. To address this issue, we review and break down the existent exercise models into categories based on exercise modality, intensity, frequency, and duration. The timing of sample collection is also compared and sorted into four distinct phases: pre-exercise (Phase I), mid-exercise (Phase II), exercise recovery (Phase III), and post-exercise (Phase IV). Finally, because the life-span of animals so are limited, small changes in animal exercise duration can corresponded to untenable amounts of human exercise. To address this limitation, we introduce the Life-Span Relative Exercise Time (RETlife span) as a method of accurately defining short-term, medium-term and long-term exercise relative to the animal’s life expectancy. Systematic organization of existent protocols and this new system of defining exercise duration will allow for a more solid framework from which researchers can extrapolate animal model data to clinical application.

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Section: Principle Of Animal Exercise Training Protocols and Sample Cmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A systematic comparison of exercise training protocols on animal models of cardiovascular capacity

Feng

Wang

et al. 2019

Life Sciences

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“…NO is a reactive gas secreted in endothelial cells by the endothelial isoform of the enzyme NO synthase, and is tonically released to control systemic vascular tone and neuronal activity in the CNS [93]. In chronic cerebral hypoperfusion models of VCI [94] and in hypertensive rats [95], it has been observed that the bioavailability of endothelium-derived NO is reduced, and that this reduction may be the cause of cognitive deficits. Further support to this hypothesis comes from studies in AD animal models, where a reduction of NO increases the negative effects of amyloid beta (Aβ) on cognition, whereas the administration of NO has a protective effect on Aβ deposition [96].…”

Section: Molecular Mechanism Of Vcimentioning

confidence: 99%

“…Many studies are now concentrating on treatments aimed at restoring NO levels at normal conditions in VCI models [92,95,97].…”

Section: Molecular Mechanism Of Vcimentioning

confidence: 99%

Vascular Cognitive Impairment: Information from Animal Models on the Pathogenic Mechanisms of Cognitive Deficits

Hort

Vališ

Kuča

et al. 2019

IJMS

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Vascular cognitive impairment (VCI) is the second most common cause of cognitive deficit after Alzheimer’s disease. Since VCI patients represent an important target population for prevention, an ongoing effort has been made to elucidate the pathogenesis of this disorder. In this review, we summarize the information from animal models on the molecular changes that occur in the brain during a cerebral vascular insult and ultimately lead to cognitive deficits in VCI. Animal models cannot effectively represent the complex clinical picture of VCI in humans. Nonetheless, they allow some understanding of the important molecular mechanisms leading to cognitive deficits. VCI may be caused by various mechanisms and metabolic pathways. The pathological mechanisms, in terms of cognitive deficits, may span from oxidative stress to vascular clearance of toxic waste products (such as amyloid beta) and from neuroinflammation to impaired function of microglia, astrocytes, pericytes, and endothelial cells. Impaired production of elements of the immune response, such as cytokines, and vascular factors, such as insulin-like growth factor 1 (IGF-1), may also affect cognitive functions. No single event could be seen as being the unique cause of cognitive deficits in VCI. These events are interconnected, and may produce cascade effects resulting in cognitive impairment.

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“…Spontaneously hypertensive stroke-prone (SHRSP) rat is a well-recognized animal model of lacunar stroke and essential hypertension in humans (17)(18)(19). 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).…”

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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Inhibition of endothelial nitric oxide synthase reverses the effect of exercise on improving cognitive function in hypertensive rats

Cited by 14 publications

References 36 publications

A systematic comparison of exercise training protocols on animal models of cardiovascular capacity

A systematic comparison of exercise training protocols on animal models of cardiovascular capacity

Vascular Cognitive Impairment: Information from Animal Models on the Pathogenic Mechanisms of Cognitive Deficits

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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