Journal of Applied Physiology, Vol 63, Issue 5 1933-1941, Copyright © 1987 by American Physiological Society
Effects of temperature on cholinergic contractility of rabbit airway muscle
D. L. Bratton, D. T. Tanaka and M. M. Grunstein
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado.
To elucidate the mechanism underlying temperature-induced changes in airway
cholinergic contractility, the effects of organ bath cooling were evaluated
in isolated rabbit airway smooth muscle (ASM) segments isometrically
contracted with methacholine (METH) (10(-8)-10(-3) M) and electrical field
stimulation (ES), wherein the ES stimulus frequency was varied between 1
and 100 Hz. Cooling from 37 to 25 degrees C produced systematic increases
(P less than 0.01) in isometric tension at various administered doses of
METH and at different levels of ES. Since the potentiated contractions to
ES significantly exceeded (P less than 0.001) the corresponding increases
in METH-induced contractility, we evaluated whether the latter was
attributed to temperature-mediated changes in intrinsic airway neuronal
acetylcholine (ACh) release. Accordingly, the effects of ASM cooling were
independently determined before and after inhibition of the Na+-K+
electrogenic pump with ouabain (10(-5) M), and depletion of intrinsic
neuronal ACh stores with hemicholinium-3 (HC-3) (10(-3) M). In the presence
of either ouabain or HC-3 the above responses to temperature reduction were
reversed, and airway cooling was associated with abrupt relaxation of ASM
segments precontracted with METH. In contrast, neither inhibition of
cyclooxygenase products with indomethacin (10(-6) M) nor cholinesterase
inhibition with neostigmine (10(-3) M) notably influenced the ASM responses
to organ bath cooling. Thus these findings demonstrate that 1) both
METH-induced and neurally mediated cholinergic contractility are augmented
during airway cooling; 2) the potentiated cholinergic responses are
attributed to enhanced presynaptic release of ACh at the airway
neuromuscular junction.(ABSTRACT TRUNCATED AT 250 WORDS)
