NONADRENERGIC RELAXATION OF THE CAT CERVICAL TRACHEA EVOKED BY STIMULATION IN THE LATERAL HYPOTHALAMIC AREA

The purpose of this study was to evaluate hypothalamic contributions t o control of tracheal tone. We found hypothalamic sites where electric al stimulation (60-90 mu A: 1 ms pulse duration: 50 Hz: 5-10 s) and mi croinjection of L-glutamate (5-50 nmol) produced tracheal relaxation r esponses along with decreased blood pressure and heart rate in anesthe tized, spontaneously breathing cats. Responsive sites were located in anterior (LHAa) and tuberal (LHAt) regions of the lateral hypothalamic area, indicating that neuronal cells in those regions are responsible for development of tracheal relaxation. In a second experiment, we ev aluated possible pathways mediating the tracheal relaxation response e licited by LHA stimulation. Tracheal relaxation was not attenuated by beta-adrenergic blockade (propranolol i.v., 0.2-0.5 mg/kg); the respon se is mediated by nonadrenergic mechanisms. Muscarinic blockade (atrop ine i.v.) at doses of 0.05-0.1 mg/kg almost abolished tracheal tone du ring spontaneous breathing, and LHA stimulation evoked a small, insign ificant reduction of tracheal tone. Cervical vagotomy completely aboli shed the tracheal tone, and LHA stimulation no longer evoked the trach eal relaxation. These results indicate the existence of a nonadrenergi c descending pathway within the vagal efferents, which is linked with behavioral control arising from LHA, and causes tracheal relaxation. C opyright (C) 1996 Elsevier Science Ireland Ltd