The emotional response to pain is also altered. Binding of GTP leads to a release of the G-protein subunit, which acts on the effector system. In this case of opioid-induced analgesia, the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane. Thus, opiates decrease intracellular cAMP by inhibiting adenylate cyclase that modulates the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline. Opiates also modulate the endocrine and immune systems.
Opiates inhibit the release of vasopressin, somatostatin, insulin and glucagon.
The exact mechanism how opioid agonists cause both inhibitory and stimulatory processes is not well understood. Clinically, stimulation of -receptors produces analgesia, euphoria, respiratory depression, miosis, decreased gastrointestinal motility, and physical dependence. Miosis is produced by an excitatory action on the autonomic segment of the nucleus of the oculomotor nerve. Respiratory depression is caused by direct action of opiate agonists on respiratory centers in the brain stem. Opiate agonists also decrease secretions from the stomach, pancreas, and biliary tract.