Perinatal exposure to environmental tobacco smoke alters cell signaling in a primate model: autonomic receptors and the control of adenylyl cyclase activity in heart and lung.

Perinatal exposure to environmental tobacco smoke (ETS) is known to have adverse effects on respiratory function in conjunction with changes in autonomic responses. In the current study, Rhesus monkeys were exposed to ETS during late gestation and in the early neonatal period. Hearts and lungs were examined for changes in beta-adrenergic and m2-muscarinic cholinergic receptors, and for alterations in adenylyl cyclase activity. Whereas there were no changes in the heart, there was robust induction of adenylyl cyclase in the lung; previous work with prenatal nicotine exposure in rodent models has shown that adenylyl cyclase induction is associated with a shift towards predominance of cholinergic over adrenergic responses. These data indicate that perinatal ETS exposure evokes changes in cells signaling that they are selective for the lung and that may ultimately reflect adverse effects at the level of physiological function.