Perinatal nicotine exposure alters AT1 and AT2 receptor expression pattern in the brain of fetal and offspring rats

Mao, Caiping; Zhang, Hong; Xiao, Daliao; Zhu, Liyan; Ding, Yang; Wu, Lei; Xu, Zhice; Zhang, Li

doi:10.1016/j.brainres.2008.09.060

Cited by 16 publications

(10 citation statements)

References 27 publications

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“…In female rats following ovariectomy, estrogen replacement significantly down-regulated AT1R and up-regulated AT2R expression in the adrenal glands 45 and kidneys 44 . Interleukin-6 treatment 46 , nicotine exposure 47 , and chronic hypoxia 48 have also been demonstrated to evoke an inverse expression pattern of AT1R and AT2R. In the current study, we found a highly negative correlation between AT1R and AT2R protein expression from fetus to six weeks of age.…”

Section: Discussionsupporting

confidence: 65%

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Gao

Chao

Parbhu

et al. 2012

J Renin Angiotensin Aldosterone Syst

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In the current experiment, we determined AT2R and AT1R protein expression by Western blot analysis in developing normal mice. The results indicate that, (1) in all detected brain regions and in the spinal cord, adult mice exhibited significantly higher AT2R expression and lower AT1R expression in total protein extracts compared to fetuses and neonates; (2) other major organs, including heart, lung, liver, and kidney, exhibited the same expression pattern as the brain and spinal cord; (3) reciprocal changes in AT2R and AT1R expression were found in the total protein extracts from the brainstems of mice from one day prenatal to six weeks of age. There was a negative correlation between AT2R and AT1R protein expression; (4) in both membrane and cytosolic fractions from the brainstem, adult mice exhibited higher AT2R and lower AT1R expression than did fetuses and neonates; (5) in the brainstem, there were no significant differences in AT2R and AT1R mRNA levels among fetal, neonatal, and adult mice. The above results reconfirmed our previous finding in rats that adult animals have higher AT2R and lower AT1R expression compared to fetuses and neonates. These data imply an involvement of AT1R in fetal development and of AT2R in adult function.

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Section: Discussionsupporting

confidence: 65%

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Gao

Chao

Parbhu

et al. 2012

J Renin Angiotensin Aldosterone Syst

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“…In addition, prenatal nicotine exposure increases blood norepinephrine levels at baseline as well as following intrave-R898 NICOTINE AND THE RAS nous administration of ANG II (147). Increased AT 1 R and decreased AT 2 R expression were observed in whole brain extracts from fetal and adult offspring rats that had been subjected to perinatal nicotine exposure (96). The downregulation of AT 2 R in the brain was shown to occur through nicotine-mediated hypermethylation of the AT 2 R promoter (90,91).…”

Section: Nicotine and The Ras In The Nervous Systemmentioning

confidence: 97%

Nicotine and the renin-angiotensin system

Oakes

Fuchs

Gardner

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

275

268

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Cigarette smoking is the single most important risk factor for the development of cardiovascular and pulmonary diseases (CVPD). Although cigarette smoking has been in constant decline since the 1950's, the introduction of e-cigarettes or electronic nicotine delivery systems 10 years ago has attracted former smokers as well as a new generation of consumers. Nicotine is a highly addictive substance, and it is currently unclear whether e-cigarettes are "safer" than regular cigarettes or whether they have the potential to reverse the health benefits, notably on the cardiopulmonary system, acquired with the decline of tobacco smoking. Of great concern, nicotine inhalation devices are becoming popular among young adults and youths, emphasizing the need for awareness and further study of the potential cardiopulmonary risks of nicotine and associated products. This review focuses on the interaction between nicotine and the renin-angiotensin system (RAS), one of the most important regulatory systems on autonomic, cardiovascular and pulmonary functions in both health and disease. The literature presented in this review strongly suggests that nicotine alters the homeostasis of the RAS by up-regulating the detrimental angiotensin converting enzyme (ACE)/Angiotensin (Ang)-II/Ang-II type 1 receptor (ATR) axis and down-regulating the compensatory ACE2/Ang-(1-7)/Mas receptor axis, contributing to the development of CVPD.

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“…Whether circulating or intrarenal levels of the RAAS are altered is not reported but increased adipose angiotensinogen expression is observed in other animal models of obesity (89) and the RAAS impacts adipose cell mass in the presence of a high fat diet (255). Central expression of the AT 1 R is increased in offspring exposed to maternal protein restriction (160) and nicotine exposure (124). Blood pressure is not increased in young adulthood in offspring exposed to perinatal nicotine (249).…”

Section: The Underlying Mechanisms That Program An Increase In Cardiomentioning

confidence: 99%

Fetal Programming and Cardiovascular Pathology

Alexander

Dasinger

Intapad

2015

Comprehensive Physiology

184

144

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Low birth weight serves as a crude proxy for impaired growth during fetal life and indicates a failure for the fetus to achieve its full growth potential. Low birth weight can occur in response to numerous etiologies that include complications during pregnancy, poor prenatal care, parental smoking, maternal alcohol consumption or stress. Numerous epidemiological and experimental studies demonstrate that birth weight is inversely associated with blood pressure and coronary heart disease. Sex and age impact the developmental programming of hypertension. In addition, impaired growth during fetal life also programs enhanced vulnerability to a secondary insult. Macrosomia, which occurs in response to maternal obesity, diabetes and excessive weight gain during gestation, is also associated with increased cardiovascular risk. Yet, the exact mechanisms that permanently change the structure, physiology and endocrine health of an individual across their lifespan following altered growth during fetal life are not entirely clear. Transmission of increased risk from one generation to the next in the absence of an additional prenatal insult indicates an important role for epigenetic processes. Experimental studies also indicate that the sympathetic nervous system, the renin angiotensin system, increased production of oxidative stress and increased endothelin play an important role in the developmental programming of blood pressure in later life. Thus, this review will highlight how adverse influences during fetal life and early development program an increased risk for cardiovascular disease including high blood pressure and provide an overview of the underlying mechanisms that contribute to the fetal origins of cardiovascular pathology.

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Perinatal nicotine exposure alters AT1 and AT2 receptor expression pattern in the brain of fetal and offspring rats

Cited by 16 publications

References 27 publications

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Nicotine and the renin-angiotensin system

Fetal Programming and Cardiovascular Pathology

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