Vagal neuroeffector mechanisms affecting transpulmonary pressure in
the intact rat.
Haselton, James R., Andrew Y. Reynolds, and Harold D. Schultz.
Department of Physiology and Biophysics, University of Nebraska
Medical Center, 600 South 42 Street, Omaha, NE 68198-4575
APStracts 2:0230A, 1995.
Studies were conducted to determine if vagal activation in the intact
anesthetized rat elicits airways smooth muscle responses attributable
to non-adrenergic, non-cholinergic transmitters. Transpulmonary
pressure (Ptr) was used as an index of airways smooth muscle tone,
and the peak inspiratory Ptr (peak Ptr) values were used for
comparison of responses. Experiments were conducted with chloralose
-urethane-anesthetized rats to assess the effects of: 1) bilateral
stimulation of the cervical vagus nerves, and 2) parasympathomimetic
and sympathomimetic agents. As expected, in untreated animals
bilateral stimulation of the vagus nerves elicited an increase in
peak Ptr of 155% (from 7.5 + 0.4 cm H2O to 11.6 + 1.2 cm H2O). The
magnitude of the response was greatest when the stimulus frequency
was >/= 40 Hz, and with stimulus pulse durations >/= 0.1 ms but =
0.25 ms. Cooling of the vagus nerves to 15 C abolished the response
of peak Ptr to vagal stimulation (40 Hz, 0.5 ms, 20 V, 30 sec). While
[beta]-adrenergic activation with isoproterenol (1 - 10 [mu]g/kg, iv)
did not alter resting peak Ptr, it did prevent vagal stimulation from
evoking an increase in peak Ptr. Prior to isoproterenol, baseline
peak Ptr was 7.6 + 0.3 cm H2O and peak Ptr during vagal stimulation
was 11.5 + 0.5 cm H2O, but in the same animals immediately following
the administration of isoproterenol peak Ptr was 7.5 + 0.4 cm H2O
before, and 8.1 + 0.2 cm H2O cm H2O during, vagal stimulation.
Nadolol (1.5 mg/kg, iv) augmented the increase in peak Ptr elicited
by vagal stimulation; vagal stimulation (40 Hz, 0.5 ms, 20 V)
increased peak Ptr from 7.9 + 0.4 to 11.4 + 0.9 cm H2O prior to
nadolol, and from 7.9 + 0.4 to 13.4 + 0.8 cm H2O after nadolol.
Methacholine (5 - 20 [mu]g/kg, iv) evoked a significant increase in
peak Ptr from 7.3 + 0.5 cm H2O to 9.6 + 0.9 cm H2O at the highest
dose only. Additional experiments were conducted to determine if a
non- adrenergic, non-cholinergic (NANC) system exists in the rat
airways. Vagal stimulation did not evoke any change in peak Ptr
following the administration of both nadolol and atropine, nor after
combined administration of nadolol, atropine, and either serotonin
aerosol or prostaglandin F2[alpha]. In another series of experiments,
conducted in rats pretreated with capsaicin one week prior to the
experiment, vagal stimulation evoked an increase in peak Ptr that was
not statistically different from that of untreated controls. On the
other hand, both the baseline heart rate and the change in heart rate
evoked by vagal stimulation in the capsaicin-pretreated rats were
significantly different from that observed in untreated rats.
Therefore, NANC systems did not appear to play an independent role in
the response of the airways to the activation of the vagus nerves.
Received 10 June 1994; accepted in final form 16 may 1995.
APS Manuscript Number A574-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.