About: Prenatal dexamethasone and postnatal high-fat diet have a synergistic effect of elevating blood pressure through a distinct programming mechanism of systemic and adipose renin

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About: Prenatal dexamethasone and postnatal high-fat diet have a synergistic effect of elevating blood pressure through a distinct programming mechanism of systemic and adipose renin–angiotensin systems Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Prenatal dexamethasone and postnatal high-fat diet have a synergistic effect of elevating blood pressure through a distinct programming mechanism of systemic and adipose renin–angiotensin systems
Creator	Li, Shih-Wen Yu, Hong-Ren Hsieh, Kai-Sheng Chen, Chih-Cheng Huang, Li-Tung Lin, I-Chun Lin, Yu-Ju Sheen, Jiunn-Ming Tain, You-Lin Tiao, Mao-Meng Tsai, Ching-Chou
Source	PMC
abstract	BACKGROUND: Hypertension may result from high-fat (HF) diet induced-obesity and overexposure to glucocorticoids in utero. Recent studies demonstrated the potent contribution of adipose tissue’s renin-angiotensin system (RAS) to systemic RAS, which plays a key role in regulating blood pressure (BP). In this study, we investigated the effects of prenatal dexamethasone (DEX) exposure and postnatal HF diet on RAS of adipose tissue. METHODS: RAS and BP of 6-month old rats exposed to prenatal DEX and/or postnatal HF diet were examined. RESULTS: Prenatal DEX plus postnatal HF exerted a synergistic effect on systolic BP. Prenatal DEX exposure suppressed plasma angiotensin (ANG) I and ANG II, whereas postnatal HF suppressed plasma ANG-(1–7) level. Prenatal DEX increased prorenin receptor and renin levels, but suppressed angiotensinogen (AGT) and angiotensin-converting-enzyme 1 (ACE1) mRNA expressions in adipose tissue. Postnatal HF increased AGT mRNA expression, but suppressed prorenin receptor, renin, ACE2, ANG II type 2 receptor (AT2R), and Mas receptor (MasR) mRNA expression levels. CONCLUSIONS: Prenatal GC exposure altered the ACE1/ANG II/ANG II type 1 receptor (AT1R) axis, whereas postnatal HF negatively impacted the ACE2/ANG-(1–7)/MasR axis. Prenatal DEX exposure and postnatal HF synergistically elevated BP through a distinct programming mechanism of systemic and adipose RAS. Adipose RAS might be a target for precise hypertension treatment. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12944-018-0701-0) contains supplementary material, which is available to authorized users.
has issue date	2018-03-14(xsd:dateTime)
bibo:doi	10.1186/s12944-018-0701-0
bibo:pmid	29540174
has license	cc-by
sha1sum (hex)	47fa3a3ddaaefacb3bf706539e89acbec03a646c
schema:url	https://doi.org/10.1186/s12944-018-0701-0
resource representing a document's title	Prenatal dexamethasone and postnatal high-fat diet have a synergistic effect of elevating blood pressure through a distinct programming mechanism of systemic and adipose renin–angiotensin systems
has PubMed Central identifier	PMC5853160
has PubMed identifier	29540174
schema:publication	Lipids Health Dis
resource representing a document's body	covid:47fa3a3ddaaefacb3bf706539e89acbec03a646c#body_text
is schema:about of	named entity 'regulating' named entity 'Hypertension' named entity 'adipose' named entity 'dexamethasone' named entity 'RAS' named entity 'overexposure' named entity 'systemic' named entity 'Hypertension' named entity 'postnatal' named entity 'prenatal' named entity 'renin-angiotensin' named entity 'fat' named entity 'blood pressure' named entity 'cDNA' named entity 'systolic pressure' named entity 'plasma' named entity 'synergistic effect' named entity 'reference genes' named entity 'AGT' named entity 'renin' named entity 'ACE2' named entity 'mRNA' named entity 'RAS' named entity 'epididymal' named entity 'statistically significant' named entity 'RAS' named entity 'ACE2' named entity 'blood pressure' named entity 'fetal development' named entity 'retroperitoneal' named entity 'mRNA' named entity 'weaned' named entity 'ACE2' named entity 'Laboratory Animals' named entity 'perirenal fat' named entity 'β-actin' named entity 'postnatal' named entity 'receptor' named entity 'saline' named entity 'retroperitoneal' named entity 'RAS' named entity 'Renin' named entity 'renin' named entity 'fat' named entity 'fat' named entity 'physical compression' named entity 'AGT' named entity 'expression of genes' named entity 'luminal' named entity 'body weight' named entity 'ACE2' named entity 'RAS' named entity 'rib cage' named entity 'intraperitoneal' named entity 'postnatal' named entity 'AGT' named entity 'fat' named entity 'angiotensin-converting' named entity 'RAS' named entity '23.5%' named entity 'angiotensinogen' named entity 'mRNA' named entity 'postnatal' named entity 'RAS' named entity 'kidney' named entity 'plasma' named entity 'AGT' named entity '2, 3' named entity 'plasma' named entity 'ACE2' named entity 'angiotensin II'

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