Developmental changes in the rat atriopeptin hormonal system.

Developmental changes in the rat atriopeptin hormonal system.
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大鼠心房肽激素系统的发育变化。

DOI:
--
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发表时间:
1987
影响因子:
15.9
通讯作者:
Philip Needleman
Philip Needleman
中科院分区:
医学1区
文献类型:
--
作者:
Yuefang Wei;Charles P. Rodi;Mark L. Day;Roger C. Wiegand;Lawrence D. Needleman;Barbara R. Cole;Philip Needleman

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We undertook a study of fetal synthesis, storage, and release of atriopeptin (AP). Plasma levels of both atriopeptin immunoreactivity (APir) and the NH2-terminal fragment of the prohormone immunoreactivity (NTFir) were very high in the fetus (4 and 20 times the maternal plasma, respectively). However, the atrial content of the AP was low, but surprisingly, ventricular content of AP was quite high (relative to the adult) in the fetus and fell postnatally. Atrial AP messenger RNA (mRNA) increased with postnatal age, whereas ventricular mRNA was extremely high in the fetus and fell rapidly after birth. High fetal plasma peptide levels may derive from the mother since infusion of exogenous atriopeptin 24 into the mother resulted in parallel increases in fetal and maternal peptide levels. Fetal plasma APir and NTFir levels partially reflect the markedly reduced total renal metabolic capacity compared with that of the adult. Plasma levels fell progressively after birth; whereas neonatal atrial content rose substantially. Plasma AP and NTF were simultaneously elevated in both the maternal and fetal circulation after vasopressin injection of the mother. The fetus can also respond to exogenous stimuli (vasopressin or indomethacin--presumably via ductal closure) and promptly release substantial amounts of peptide into its circulation. Thus, it appears that the AP hormonal system is functional during fetal life and responds avidly to increases in intracardiac pressure as does the mature animal.
具有生物活性的心房肽。
DOI: 10.1172/jci112206
发表时间: 1985
期刊: The Journal of clinical investigation
影响因子: --
作者:
Ballerman,BJ;Brenner,BM
通讯作者: Brenner,BM
DOI: 10.1016/0006-291x(86)90019-7
发表时间: 1986
影响因子: 3.1
作者:
Sen,I
通讯作者: Sen,I