Role of cholinergic neural transmission on airway resistance in the dog.
The unique contractile profiles of bronchial smooth muscle (Kondo et al., 1995) and its neural control were investigated by comparing responses of the bronchus and trachea to acute hypercapnia, stimulation of vagus efferent fibers before and after intravenous atropine, and intravenous acetylcholine in decerebrated and paralyzed dogs. During acute hypercapnia, airway resistance represented by peak airway pressure (Pedley et al., 1970) significantly increased as well as tracheal tension (Ttr). During electric stimulation of the vagal efferent fibers, Ttr increased and was sustained throughout the simulation period while the peak airway pressure was not maintained at the peak level. The peak Ttr and the airway resistance (Raw) calculated from ventilatory flow and airway pressure increased with increases in intensity of electric stimulation. Ttr reached its maximal level at an intensity 16 times of the threshold (T), while Raw became maximal at 4T. Although both the Ttr-stimulus intensity and Raw-intensity curves were shifted to the right by administration of intravenous atropine, the Raw curve shifted more to the right than the Ttr curve with the same dose of atropine. When muscular muscarinic receptors were directly stimulated by intravenous acetylcholine, Ttr once increased and then decreased promptly while peak airway pressure remained at a high level for a few minutes. These findings suggested that the bronchus is more sensitive to vagal efferent stimulation and susceptible to competitive antagonist of actylcholine than the trachea. In conclusion, the contractile profiles of the fifth-order bronchus we have reported (Kondo et al., 1995) were reflected in airway resistance, and the neuromuscular junction may be the site of adaptation of bronchoconstrictor response to motor nerve adaptation.
Kondo
T
T
Department of Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan. tetsuri@is.icc.u-tokai.ac.jp
Kobayashi
I
I
Hayama
N
N
Tazaki
G
G
Ohta
Y
Y
D000109:Acetylcholine / Q000494:pharmacology; D000208:Acute Disease; D000403:Airway Resistance; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D016084:Bronchoconstriction / Q000187:drug effects / Q000502:physiology*; D002799:Cholinergic Fibers / Q000502:physiology*; D004285:Dogs; D004558:Electric Stimulation; D006935:Hypercapnia / Q000503:physiopathology; D009130:Muscle, Smooth / Q000294:innervation* / Q000502:physiology; D009476:Neurons, Efferent / Q000502:physiology; D010276:Parasympatholytics / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014132:Trachea / Q000294:innervation* / Q000502:physiology; D014630:Vagus Nerve / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
D010276:Parasympatholytics; D014665:Vasodilator Agents; D001285:Atropine; D000109:Acetylcholine