Abstract:Atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide belong to a family of hormones that have diuretic, natriuretic and vasodepressor activity and play a part in pressure and volume homeostasis in adults. As little is known about the natriuretic peptides during cardiac maturation, this review summarizes current knowledge about the early expression of components of the natriuretic peptide system in the heart during embryonic and fetal development. The data indicate a functional i… Show more
“…As reported by Walther et al (29), the natriuretic peptides appear to respond to similar stimuli, and to perform similar cardiovascular functions during development as they do in adults. The fetal natriuretic peptides (30,31) can react to volume loading, hyperosmolality, and vasoconstrictors Ang II, phenylephrine, and endothelin in a manner similar to that in the adult heart; however, ANP and BNP respond differently to short-term and long-term volume load in the fetal circulation (32).…”
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.
“…As reported by Walther et al (29), the natriuretic peptides appear to respond to similar stimuli, and to perform similar cardiovascular functions during development as they do in adults. The fetal natriuretic peptides (30,31) can react to volume loading, hyperosmolality, and vasoconstrictors Ang II, phenylephrine, and endothelin in a manner similar to that in the adult heart; however, ANP and BNP respond differently to short-term and long-term volume load in the fetal circulation (32).…”
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.
“…Histological and immunocytochemical studies, as well as in situ hybridization analysis, confirmed expression of the ANP gene in human [32] and ovine fetal heart [33]. Moreover, whereas ANP [34] and ANP mRNA [35] are present throughout the heart in the early embryological stages of development, the ventricular representation regresses markedly towards the later developmental phases [35] (for review see [36]). Mature ANP is a 28-amino-acid peptide hormone with a molecular mass of 3080.5 kDa (C 127 H 203 N 45 O 39 S 3 ).…”
Since the discovery of atrial natriuretic peptide, the unravelling of the natriuretic peptide system has been a story of scientific success. However, bridging the gap between bench and bedside has proved difficult, and as yet has not provided any major clinical progress. In this review we will first give a detailed outline of the key elements constituting the natriuretic peptide system. Secondly, we will briefly explain the underlying rationale, basic concepts and evidence behind currently pursued strategies to potentiate the natriuretic peptide system. Thirdly, we will highlight some of the problems that have so far hindered successful translation of these theoretically viable treatment options into tangible clinical progress.
“…5A,C,E) (Moorman and Christoffels, 2003). Nppa is a hormone involved in the homeostatic regulation of blood pressure and volume in adults (Walther et al, 2002). Previous reports have shown that Tbx2 downregulates expression of an Nppa reporter in transgenic mouse embryos at 10.5 dpc (Habets et al, 2002).…”
Section: Myocardial Differentiation and Patterning In Tbx2 Tm1pamentioning
Tbx2 is a member of the T-box transcription factor gene family,and is expressed in a variety of tissues and organs during embryogenesis. In the developing heart, Tbx2 is expressed in the outflow tract, inner curvature, atrioventricular canal and inflow tract, corresponding to a myocardial zone that is excluded from chamber differentiation at 9.5 days post coitus (dpc). We have used targeted mutagenesis in mice to investigate Tbx2 function. Mice heterozygous for a Tbx2 null mutation appear normal but homozygous embryos reveal a crucial role for Tbx2 during cardiac development. Morphological defects are observed in development of the atrioventricular canal and septation of the outflow tract. Molecular analysis reveals that Tbx2 is required to repress chamber differentiation in the atrioventricular canal at 9.5 dpc. Analysis of homozygous mutants also highlights a role for Tbx2 during hindlimb digit development. Despite evidence that TBX2 negatively regulates the cell cycle control genes Cdkn2a, Cdkn2b and Cdkn1a in cultured cells, there is no evidence that loss of Tbx2 function during mouse development results in increased levels of p19ARF, p16INK4a,p15INK4b or p21 expression in vivo, nor is there evidence for a genetic interaction between Tbx2 and p53.
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