Induced fetal depressor or pressor responses associated with c-fos by intravenous or intracerebroventricular losartan

Shi, Lijun; Yao, Jiaming; Koos, Brian J.; Xu, Zhice

doi:10.1016/j.devbrainres.2004.07.012

Cited by 5 publications

(6 citation statements)

References 27 publications

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“…This indicates that fetal brain AT1R plays an important role in physiological or pathophysiological responses to the actions of central Ang II. Of note, a high dose of icv losartan itself also increased fetal arterial pressure, which differed from observations in adult animals with similar treatments (Shi et al, 2004b). Although we do not have data to explain the difference, abundant fetal brain AT2R could be one of the causes for different phenomenon observed after central application of the Ang II receptor antagonist.…”

Section: Functional Development Of the Fetal Brain Rascontrasting

confidence: 86%

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Mao

Shi

et al. 2009

Progress in Neurobiology

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Since the concept of fetal origins of adult diseases was introduced in 1980s, the development of the renin-angiotensin system (RAS) in normal and abnormal patterns has attracted attention. Recent studies have shown the importance of the fetal RAS in both prenatal and postnatal development. This review focuses on the functional development of the fetal brain RAS, and ontogeny of local brain RAS components in utero. The central RAS plays an important role in the control of fetal cardiovascular responses, body fluid balance, and neuroendocrine regulation. Recent progress has been made in demonstrating that altered fetal RAS development as a consequence of environmental insults may impact on "programming" of hypertension later in life. Given that the central RAS is of equal importance to the peripheral RAS in cardiovascular regulation, studies on the fetal brain RAS development in normal and abnormal patterns could shed light on "programming" mechanisms of adult cardiovascular diseases in fetal origins.

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Section: Functional Development Of the Fetal Brain Rascontrasting

confidence: 86%

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Mao

Shi

et al. 2009

Progress in Neurobiology

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“…The data showed that foetal plasma Ang II levels were decreased, and aldosterone concentrations were increased. Although AVP, ACTH, ANP, and PGE can also affect cardiovascular responses and body fluid balance, 14,15 we did not find any change in these humoral levels in the foetus after administration of atropine.…”

Section: Tablecontrasting

confidence: 67%

“…volume. 14,15 In the present study, we measured these seven hormones or compounds in the foetal circulation after the treatment with atropine. The data showed that foetal plasma Ang II levels were decreased, and aldosterone concentrations were increased.…”

Section: Tablementioning

confidence: 99%

“…Among many hormones or compounds, angiotensin (Ang), arginine vasopressin (AVP), adrenocorticotrophic hormone (ACTH), atrial natriuretic peptide (ANP), aldosterone, and prostaglandin E (PGE) have been considered critical in the control of either cardiovascular activity or vascular volume. 14,15 Therefore, these hormones and compounds were determined in the present foetal study in vivo and in utero. The present study used the muscarinic (M) receptor antagonist in determination of the role of cholinergic mechanisms in hormonal and vascular regulation in the ovine foetus.…”

Section: Introductionmentioning

confidence: 99%

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Muscarinic effects and foetal cardiovascular and hormonal responses in utero

Zheng

Yang

Cao

et al. 2009

J Renin Angiotensin Aldosterone Syst

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“…AT2 receptors do not appear to be involved, because icv injection of PD123319, the specific antagonist of AT2 receptor, did not affect Ang II-induced cardiovascular effects. This indicates that the central RAS and AT1, but not AT2 receptor, are critically involved in the regulation of arterial pressure in the near-term fetal sheep (18). In the near-term ovine fetus, AT1 receptors but not AT2 receptors (19) contribute to dipsogenic and pressor responses, as well as arginine vasopressin (AVP) release.…”

Section: Hormonal Regulation Of Fluid Homeostasis Fetal Renin-angiotementioning

confidence: 99%

Fetal development of regulatory mechanisms for body fluid homeostasis

Guan

Mao

Feng

et al. 2008

Braz J Med Biol Res

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The balance of body fluids is critical to health and the development of diseases. Although quite a few review papers have shown that several mechanisms, including hormonal and behavioral regulation, play an important role in body fluid homeostasis in adults, there is limited information on the development of regulatory mechanisms for fetal body fluid balance. Hormonal, renal, and behavioral control of body fluids function to some extent in utero. Hormonal mechanisms including the renin-angiotensin system, aldosterone, and vasopressin are involved in modifying fetal renal excretion, reabsorption of sodium and water, and regulation of vascular volume. In utero behavioral changes, such as fetal swallowing, have been suggested to be early functional development in response to dipsogens. Since diseases, such as hypertension, can be traced to fetal origin, it is important to understand the development of fetal regulatory mechanisms for body fluid homeostasis in this early stage of life. This review focuses on fetal hormonal, behavioral, and renal development related to regulation of body fluids in utero.

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Induced fetal depressor or pressor responses associated with c-fos by intravenous or intracerebroventricular losartan

Cited by 5 publications

References 27 publications

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Muscarinic effects and foetal cardiovascular and hormonal responses in utero

Fetal development of regulatory mechanisms for body fluid homeostasis

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