Nonadrenergic relaxation of the cat cervical trachea evoked by stimulation in the lateral hypothalamic area

Abstract

The purpose of this study was to evaluate hypothalamic contributions to control of tracheal tone. We found hypothalamic sites where electrical stimulation (60–90 μA: 1 ms pulse duration: 50 Hz: 5–10 s) and microinjection of l-glutamate (5–50 nmol) produced tracheal relaxation responses along with decreased blood pressure and heart rate in anesthetized, 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 evaluated possible pathways mediating the tracheal relaxation response elicited by LHA stimulation. Tracheal relaxation was not attenuated by β-adrenergic blockade (propranolol i.v., 0.2–0.5 mg/kg); the response is mediated by nonadrenergic mechanisms. Muscarinic blockade (atropine i.v.) at doses of 0.05–0.1 mg/kg almost abolished tracheal tone during spontaneous breathing, and LHA stimulation evoked a small, insignificant reduction of tracheal tone. Cervical vagotomy completely abolished the tracheal tone, and LHA stimulation no longer evoked the tracheal relaxation. These results indicate the existence of a nonadrenergic descending pathway within the vagal efferents, which is linked with behavioral control arising from LHA, and causes tracheal relaxation.