Reflex activation of postganglionic vasoconstrictor neurones supplying skeletal muscle by stimulation of arterial chemoreceptors via non-nicotinic synaptic mechanisms in sympathetic ganglia

Abstract

Postganglionic sympathetic neurones supplying skeletal muscle and skin can be activated from the preganglionic site via cholinergic nicotinic, muscarinic and noncholinergic synaptic mechanisms. The experiments described in this paper were designed in order to show that postganglionic vasoconstrictor neurones supplying skeletal muscle can be activated by the naturally occurring discharge pattern in preganglionic axons when the nicotinic transmission is blocked. For this purpose, the activity was recorded simultaneously from postganglionic vasoconstrictor axons supplying skeletal muscle and vasoconstrictor axons supplying hairy skin. The preganglionic neurones were driven reflexly by stimulation of the arterial chemoreceptors. 1) During blockade of nicotinic transmission muscle vasoconstrictor neurones were activated via the CNS during stimulation of arterial chemoreceptors. This activation is either generated by muscarinic action of released acetylcholine or by a noncholinergic synaptic mechanism. 2) Postganglionic cutaneous vasoconstrictor neurones were inhibited during stimulation of arterial chemoreceptors. During blockade of cholinergic nicotinic transmission these neurones were not activated reflexly by stimulation of arterial chemoreceptors although they received inputs via cholinergic muscarinic and noncholinergic synaptic mechanisms. 3) The results illustrate that postganglionic vasoconstrictor neurones supplying skeletal muscle can not only be activated via non-nicotinic synaptic mechanisms through synchronous repetitive electrical stimulation of preganglionic axons but also by the discharge pattern produced in preganglionic neurones during stimulation of arterial chemoreceptors.

Chemical Coding for Cardiovascular Sympathetic Preganglionic Neurons in Rats

“…It has been argued elsewhere, on the basis of physiological experiments, that two functional classes of SPN innervate vasomotor postganglionic neurons (Jänig et al, 1983; Jänig, 2005; McAllen et al, 2005): these have been termed ‘regular’ and ‘accessory’ (McAllen et al, 2005). The ‘regular’ pathway provides resting tone, is strongly activated by baroreceptor unloading and communicates with ganglion cells by conventional nicotinic transmission (Henderson and Ungar, 1978; Jänig, 1995).…”

“…The ‘regular’ pathway provides resting tone, is strongly activated by baroreceptor unloading and communicates with ganglion cells by conventional nicotinic transmission (Henderson and Ungar, 1978; Jänig, 1995). By contrast, the ‘accessory’ preganglionic pathway may not drive much basal tone, but it is strongly stimulated by arterial chemoreceptors and can activate vasoconstrictor pathways by non-nicotinic transmission (Henderson and Ungar, 1978; Jänig et al, 1983, 1984). Physiologically, when nicotinic transmission is intact, non-nicotinic actions are likely to provide excitatory modulation rather than direct drive.…”

“…In both cases the action was specific to vasoconstrictor pathways (muscle, cutaneous), and did not affect non-cardiovascular pathways (pilomotor, sudomotor) (Blumberg and Janig, 1983; Jänig et al, 1984). Intriguingly, these putative peptidergic actions may be driven by central and preganglionic pathways that are functionally distinct from those carrying most ongoing vasomotor tone (Henderson and Ungar, 1978; Janig et al, 1983; Jänig, 2006). Elucidation of this matter would be greatly helped by identification of the candidate peptide.…”

Muscarinic and ganglionic blocking properties of atropine compounds in vivo and in vitro: time dependence and heart rate effects

“…In addition, mtimuscarinic agents, especially quaternary ammonium compounds, have also been reported to have ganglionic blocking properties (MacDermott et al 1986;Armour 1983Armour , 1988Janig et al 1983;Gross 1988;Brown 1990;Dujic et al 1993). Very small doses of atropine sulfate and methylatropine nitrate can reduce heart rate and cause dysrhythmias such as atrioventricular (AV) dissociation, atrial ectopy, and supraventricular rhythms with P-wave inversion in healthy, young, human volunteers (Dauchot and Gravenstein 1970;Lbnnerholm and Widerlov 19'75).…”

A Neglected ‘Accessory’ Vasomotor Pathway: Implications for Blood Pressure Control

“…We can distinguish them because their high electrical threshold shows that their axons are unmyelinated (although this, itself, need have no physiological consequence). These neurons do not appear to be responsible for normal 1 : 1 ganglionic transmission, which is attributable to the ‘regular’ preganglionic neurons with myelinated axons 11 . However, they converge upon the same vasomotor ganglion cells and, thus, may also be classified as vasomotor 6 .…”