High salt diet elevates the mean arterial pressure of SLC14α1 gene depletion mice

Wang, Song; Liu, Jinshu; Cai, Hongwei; Liu, Keyuan; He, Yayu; Liu, Shuxiang; Guo, Yingze; Guo, Lirong

doi:10.1016/j.lfs.2020.117751

Cited by 2 publications

(2 citation statements)

References 22 publications

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“…In order to further verify the potential mechanisms of VK2 for salt-sensitive hypertension, we supplemented VK2 to intervene high-salt induced mice, and detected the characteristics of gut bacteria by 16S rRNA analysis. Some studies have shown that high-salt diet (8% NaCl) for 4 weeks can cause hypertension in mice (22,23). The results of animal experiment showed that VK2 supplementation protected blood pressure and aortic vessels in salt-induced mice.…”

Section: Discussionmentioning

confidence: 99%

Network and 16S rRNA Sequencing-Combined Approach Provides Insightal Evidence of Vitamin K2 for Salt-Sensitive Hypertension

Liu

Chen

et al. 2021

Front. Nutr.

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Vitamin K2 (VK2), found to act to treat hypertension, has been widely used in the food and pharmaceutical industries nowadays. However, the potential targets and molecular mechanisms of VK2 for salt-sensitive hypertension have not been fully investigated. Therefore, the study aimed to investigate the potential molecular mechanisms of VK2 for salt-sensitive hypertension using network pharmacology and 16S rRNA sequencing strategy. The network pharmacology-based findings from KEGG enrichment analysis revealed that VK2-treated salt-sensitive hypertension was mechanically associated with the complement and coagulation cascades, calcium signaling pathway, renin–angiotensin system, etc. A total of 29 different bacteria in an animal experiment after VK2 supplementation were screened and functionally enriched using PICRUSt2. Additionally, 10 signaling pathways were identified in which the renin–angiotensin system was found to be the potential molecular mechanisms with the greatest change in multiple and statistical significance. Moreover, the results of the renin–angiotensin system-related protein expression exhibited VK2-inhibited renin–angiotensin system in salt-induced hypertensive mice, which significantly verified the previous biological and functional prediction analysis. Finally, spearman correlation analysis showed the different bacteria such as Dubosiella, Ileibacterium, etc., had a positive or negative correlation with renin–angiotensin system-related proteins in salt-induced mice. In conclusion, the potential molecular mechanisms of VK2 for salt-sensitive hypertension may be beneficially achieved by the specific inhibition of the renin–angiotensin system, contributing to the development for a new preventive strategy of salt-sensitive hypertension.

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Section: Discussionmentioning

confidence: 99%

Network and 16S rRNA Sequencing-Combined Approach Provides Insightal Evidence of Vitamin K2 for Salt-Sensitive Hypertension

Liu

Chen

et al. 2021

Front. Nutr.

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“…Once in the circulatory system, Na is widely distributed throughout the organism, accessing circumventricular brain structures, which lack a blood–brain barrier, via fenestrated capillaries [ 55 , 56 ], and accessing cerebrospinal fluid (CSF) via ion transporters (e.g., ENaC) in epithelial cells of the choroid plexus [ 57 , 58 , 59 , 60 ]. Blood and CSF both have a [Na+] concentration of 144 mOsm/L [ 61 ].…”

Section: Behavioral Mechanism: Salt Intakementioning

confidence: 99%

Sodium Homeostasis, a Balance Necessary for Life

et al. 2023

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Body sodium (Na) levels must be maintained within a narrow range for the correct functioning of the organism (Na homeostasis). Na disorders include not only elevated levels of this solute (hypernatremia), as in diabetes insipidus, but also reduced levels (hyponatremia), as in cerebral salt wasting syndrome. The balance in body Na levels therefore requires a delicate equilibrium to be maintained between the ingestion and excretion of Na. Salt (NaCl) intake is processed by receptors in the tongue and digestive system, which transmit the information to the nucleus of the solitary tract via a neural pathway (chorda tympani/vagus nerves) and to circumventricular organs, including the subfornical organ and area postrema, via a humoral pathway (blood/cerebrospinal fluid). Circuits are formed that stimulate or inhibit homeostatic Na intake involving participation of the parabrachial nucleus, pre-locus coeruleus, medial tuberomammillary nuclei, median eminence, paraventricular and supraoptic nuclei, and other structures with reward properties such as the bed nucleus of the stria terminalis, central amygdala, and ventral tegmental area. Finally, the kidney uses neural signals (e.g., renal sympathetic nerves) and vascular (e.g., renal perfusion pressure) and humoral (e.g., renin–angiotensin–aldosterone system, cardiac natriuretic peptides, antidiuretic hormone, and oxytocin) factors to promote Na excretion or retention and thereby maintain extracellular fluid volume. All these intake and excretion processes are modulated by chemical messengers, many of which (e.g., aldosterone, angiotensin II, and oxytocin) have effects that are coordinated at peripheral and central level to ensure Na homeostasis.

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High salt diet elevates the mean arterial pressure of SLC14α1 gene depletion mice

Cited by 2 publications

References 22 publications

Network and 16S rRNA Sequencing-Combined Approach Provides Insightal Evidence of Vitamin K2 for Salt-Sensitive Hypertension

Network and 16S rRNA Sequencing-Combined Approach Provides Insightal Evidence of Vitamin K2 for Salt-Sensitive Hypertension

Sodium Homeostasis, a Balance Necessary for Life

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