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Fetal hypothalamus

The major mechanism that may be operating to connect maternal stress during pregnancy to postnatal psychopathology involves effects of maternal stress hormones on development of the fetal brain, particularly of the fetal hypothalamus—pituitary—... [Pg.224]

AVP is synthesized in the fetal hypothalamus. In addition to its role in altering gene expression (e.g., POMC), plasma AVP levels also increase in response to fetal hypoxia-ischemia (30,70,71). The release of AVP is not mediated by peripheral chemoreceptor mechanisms and therefore is unlikely to contribute to the rapid cardiovascular changes at the onset of hypoxia (see above) (30). Exogenously administered AVP produces hypertension, peripheral vasoconstriction, and bradycardia (71-73), although the contribution of hypoxia-stimulated increases in AVP to the redistribution of fetal CVO is uncertain (74,75). Endothehal VI receptors mediate an AVP vasodUatory effect, which means that the net effect of AVP on the cardiovascular system is likely to reflect an integrated picture of vasoconstriction from a number of vascular beds, modulated by endothelium-dependent vasodUatory mechanisms (76). [Pg.216]

GH deficiency can have a genetic basis or can be acquired as a result of damage to the pituitary or hypothalamus by a tumor, infection, surgery, or radiation therapy. In childhood, GH deficiency presents as short stature and adiposity. (Neonates with isolated GH deficiency are of normal size at birth, presumably because fetal GH is not required for normal... [Pg.827]

A female-specific 15(3 hydroxylase acts on steroid sulfates such as corticosterone sulfate and forms the major urinary excretion product of that hormone in female rats.292 These sex-specific differences in enzymes are thought to be related to secretions of growth hormone that are in turn controlled by the "programming" of the hypothalamus by androgen during the neonatal period in rats272 or during human fetal development. [Pg.1260]

Estrogens have a number of functions and not only feminization. Sites of (human) expression include the ovaries, testes, placenta, fetal (but not adult) liver, adipose tissue, chondrocytes and osteoblasts of bone, vasculature smooth muscle, and several sites in brain, including parts of the hypothalamus, limbic system, and cerebral cor-tex °. As discussed later, regulatory mechanisms differ considerably in these tissues. P450 19A1 is also expressed in some tumors, particularly those derived from these tissues. [Pg.451]

S X rd 0 IV/IM/nasal. Short half-life (3-5 min.). Potential for uterine tetany or rupture, trauma to infant, post -delivery uterine atony. Prolonged infusion (>24h) may cause water intoxication (antidiuretic activity). Potentiates hypertensive effects of other drugs. May cause stroke/hemorrhage, fetal distress. Synthetic oxytocin mimics the effects of endogenous oxytocin which is released from the hypothalamus. [Pg.149]


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See also in sourсe #XX -- [ Pg.216 ]




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Fetal

Hypothalamus

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