3. AUTONOMIC NERVOUS SYSTEMS
117
the swim bladder in teleosts, and possibly to accessory digestive organs
and to blood vessels in this region. The innervation of the heart has
been reviewed by Nicol (1952) and more recently by Johansen and
Martin ( 1965). ( See also Chapter 4 by Randall, this volume.) The evidence
for a cholinergic vagal supply to the heart, causing a reduction in the rate
of beating, is so overwhelmingly strong that no further comment is
needed. The consensus has been that the vagi do not contain cardiac
augmentor or accelerator fibers, whether of sympathetic or parasympathetic origin (but see Section 111, B ) , and it is well established that
there are no distinct sympathetic nerves innervating the heart directly.
Jullien and Ripplinger ( 1957) found that after degenerative sections
made high in the vagal trunk stimulation of the vagal cardiac branches
still caused negative chronotropic and inotropic responses in teleosts,
indicating that the ganglionic synapses in the ~ a g a l
pathway occur within
the vagal trunk itself. They also observed that the heart rate was slow
and that arrhythmias were common in bivagotomized tench and that
the heart returned to a fast, regular beat after atropine treatment. They
suggested that the vagal postganglionic cell bodies are tonically active,
holding the heart muscle under an inhibitory drive, and that the activity
of the neurons is normally inhibited by fibers from the central nervous
system running in the vagi, a suggestion which deserves further
consideration.
A further observation made by Jullien and Ripplinger is also worth
reconsidering. In a series of papers around 1950 (summarized in Jullien
and Ripplinger, 1957), they provided evidence for a unique system of
noncholinergic “negative tonotropic” nerve fibers in the vagal supply to
the teleost heart. The crux of their argument is that in nonbeating hearts,
e.g., after treatment with acetylcholine, stimulation of the vagus causes
elongation of the heart (Fig. 3a); on the other hand, in hearts treated
with atropine, stimulation of the vagi causes elongation of the heart
when all signs of negative inotropic and chronotropic responses have
vanished (Fig. 3b). Since their recordings have been made by attaching
the heart to a kymograph lever in situ, leaving the heart attached to the
body by the large veins alone, one might suggest that the “tonotropic”
responses represent inhibition of venous smooth muscle tone. This
suggestion is striking enough but is perhaps more acceptable than the
alternative that the cardiac muscle cells are in a condition of tonus
which is not related to cardiac action potential activity.
The vagal innervation of the gut of teleosts and selachians has been
reviewed by Nicol (1959), Barrington ( 1957), and Campbell and Burnstock ( 1968). All reviewers agree that stimulation of the vagi causes contraction of the stomach, but not of the intestine, in those animals possess-
117
the swim bladder in teleosts, and possibly to accessory digestive organs
and to blood vessels in this region. The innervation of the heart has
been reviewed by Nicol (1952) and more recently by Johansen and
Martin ( 1965). ( See also Chapter 4 by Randall, this volume.) The evidence
for a cholinergic vagal supply to the heart, causing a reduction in the rate
of beating, is so overwhelmingly strong that no further comment is
needed. The consensus has been that the vagi do not contain cardiac
augmentor or accelerator fibers, whether of sympathetic or parasympathetic origin (but see Section 111, B ) , and it is well established that
there are no distinct sympathetic nerves innervating the heart directly.
Jullien and Ripplinger ( 1957) found that after degenerative sections
made high in the vagal trunk stimulation of the vagal cardiac branches
still caused negative chronotropic and inotropic responses in teleosts,
indicating that the ganglionic synapses in the ~ a g a l
pathway occur within
the vagal trunk itself. They also observed that the heart rate was slow
and that arrhythmias were common in bivagotomized tench and that
the heart returned to a fast, regular beat after atropine treatment. They
suggested that the vagal postganglionic cell bodies are tonically active,
holding the heart muscle under an inhibitory drive, and that the activity
of the neurons is normally inhibited by fibers from the central nervous
system running in the vagi, a suggestion which deserves further
consideration.
A further observation made by Jullien and Ripplinger is also worth
reconsidering. In a series of papers around 1950 (summarized in Jullien
and Ripplinger, 1957), they provided evidence for a unique system of
noncholinergic “negative tonotropic” nerve fibers in the vagal supply to
the teleost heart. The crux of their argument is that in nonbeating hearts,
e.g., after treatment with acetylcholine, stimulation of the vagus causes
elongation of the heart (Fig. 3a); on the other hand, in hearts treated
with atropine, stimulation of the vagi causes elongation of the heart
when all signs of negative inotropic and chronotropic responses have
vanished (Fig. 3b). Since their recordings have been made by attaching
the heart to a kymograph lever in situ, leaving the heart attached to the
body by the large veins alone, one might suggest that the “tonotropic”
responses represent inhibition of venous smooth muscle tone. This
suggestion is striking enough but is perhaps more acceptable than the
alternative that the cardiac muscle cells are in a condition of tonus
which is not related to cardiac action potential activity.
The vagal innervation of the gut of teleosts and selachians has been
reviewed by Nicol (1959), Barrington ( 1957), and Campbell and Burnstock ( 1968). All reviewers agree that stimulation of the vagi causes contraction of the stomach, but not of the intestine, in those animals possess-