Perinatal cocaine exposure impairs myocardial beta-adrenoceptor signaling in the neonatal rat.

Perinatal cocaine exposure impairs myocardial beta-adrenoceptor signaling in the neonatal rat.
复制标题

围产期可卡因暴露会损害新生大鼠的心肌β-肾上腺素受体信号传导。

DOI:
10.1097/00000539-200001000-00012
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发表时间:
2000
影响因子:
5.7
通讯作者:
Sun,LS
Sun,LS
中科院分区:
医学2区
文献类型:
--
作者:
Sun,LS

文献摘要

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Cardiac dysfunction occurs in infants with prenatal cocaine exposure, and gestational cocaine exposure induces presynaptic and postsynaptic changes in the central monoaminergic receptor pathways. The hypothesis of this study is that prenatal cocaine exposure adversely affects the peripheral adrenergic receptor (βAR) signaling pathway in the neonatal rat heart. Timed pregnant rats received daily intragastric treatment with saline or cocaine 20 mg/kg or 60 mg/kg from Gestational Day 2 until parturition. After birth, nursing mothers either continued to receive the same treatment or received no treatment. Adenylyl cyclase activity, βAR density, and the amount of immunoreactive G proteins were measured in myocardial membranes obtained from the offspring on Postnatal Day 1 or 7. On Postnatal Day 1, prenatal cocaine exposure increased the βAR number but did not affect isoproterenol-stimulated adenylyl cyclase activity. On Postnatal Day 7, perinatal cocaine exposure significantly attenuated isoproterenol-stimulated adenylyl cyclase activity in the absence of βAR up-regulation. Prenatal cocaine exposure also significantly increased Gi protein and reduced GTP-stimulated adenylyl cyclase activity in Postnatal Day 1 cocaine (20 mg/kg) pups compared with saline (P< 0.05). Therefore, perinatal cocaine exposure impaired the myocardial βAR-cAMP signaling pathway during the first week of postnatal life in the rat.ImplicationsThis study shows that maternal cocaine use during pregnancy impairs the β-adrenoceptor signaling pathway in the rat during the first week of life. Abnormal cardiac function in the cocaine-exposed neonate may be related to a defect in β-adrenoceptors, because they regulate cardiac function.