Perinatal exposure to environmental tobacco smoke induces adenylyl cyclaseand alters receptor-mediated cell signaling in brain and heart of neonatalrats

Perinatal exposure to environmental tobacco smoke (ETS) has adverse effects on neurobehavioral development. In the current study, rats were exposed to ETS during gestation, during the early neonatal period, or both. Brains an d hearts were examined for alterations in adenylyl cyclase (AC) activity an d for changes in beta -adrenergic and m2-muscarinic cholinergic receptors a nd their linkage to AC. ETS exposure elicited induction of total AC activit y as monitored with the direct enzymatic stimulant, forskolin. In the brain , the specific coupling of beta -adrenergic receptors to AC was inhibited i n the ETS groups, despite a normal complement of beta -receptor binding sit es. In the heart, ETS evoked a decrease in m2-receptor expression. In both tissues, the effects of postnatal ETS, mimicking passive smoking, were equi valent to (AC) or greater than (m2-receptors) those seen with prenatal ETS mimicking active smoking: the effects of combined prenatal and postnatal ex posure were equivalent to those seen with postnatal exposure alone. These d ata indicate that ETS exposure evokes changes in cell signaling that recapi tulate those caused by developmental nicotine treatment. Since alterations in AC signaling are known to affect cardiorespiratory function, the present results provide a mechanistic link reinforcing the participation of ETS ex posure, including postnatal ETS, in disturbances culminating in events like Sudden Infant Death Syndrome. (C) 2001 Elsevier Science B.V. All rights re served.