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

Abstract

1. Distinct from 'regular' sympathetic preganglionic neurons, there exists a population of 'accessory' preganglionic neurons. The latter are distinguishable by their unmyelinated axons and their different functional properties. They synapse on the same ganglion cells. 2. Ongoing sympathetic activity is driven by 'regular' preganglionic neurons. 3. 'Accessory' preganglionic neurons drive hexamethonium-resistant ganglionic transmission: part of this is muscarinic and part not (possibly peptidergic or nitrergic). 4. 'Accessory' preganglionic neurons supply cardiovascular (vasomotor, cardiac, adrenal), but apparently not other, sympathetic pathways. 5. 'Accessory' preganglionic neurons are activated by arterial chemoreceptors. 6. Brief activation of 'accessory' preganglionic neurons potentiates ongoing post-ganglionic activity for tens of minutes by an action at the ganglion. This is probably by enabling previously subthreshold excitatory post-synaptic potentials to trigger action potentials. 7. Evidence is presented that microinjections of GABA into the rostral ventrolateral medulla activate the 'accessory' pathway while inhibiting the 'regular' pathway. 8. A role for this 'accessory' pathway in the long-term control of blood pressure in health and disease is predicted, but still untested.

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).…”

NEURAL, HORMONAL and RENAL INTERACTIONS IN LONG‐TERM BLOOD PRESSURE CONTROL

“…Data from a range of experimental paradigms were presented at this conference that supported the notion that neural mechanisms contribute to long‐term blood pressure control and to the pathogenesis of hypertension in some clinical and experimental models 3,5–10 . There was considerable interest in the nature of the central and peripheral mechanisms involved 11–15 . There have also been recent advances in our understanding of the renal mechanisms that contribute to long‐term blood pressure control, dominated by extrinsic and intrinsic neurohumoral mechanisms and their interactions with the intrinsic pressure natriuresis mechanism 16–18 …”

“…3,[5][6][7][8][9][10] There was considerable interest in the nature of the central and peripheral mechanisms involved. [11][12][13][14][15] There have also been recent advances in our understanding of the renal mechanisms that contribute to long-term blood pressure control, dominated by extrinsic and intrinsic neurohumoral mechanisms and their interactions with the intrinsic pressure natriuresis mechanism. [16][17][18]…”

Alterations in the Brainstem Preautonomic Circuitry May Contribute to Hypertension Associated with Metabolic Syndrome

“…Another possibility is that the presumed increase in GABAergic neurotransmission activates an "accessory" vasomotor pathway originating from the rostral VLM (McAllen et al, 2005). This pathway is thought to activate "accessory" sympathetic preganglionic neurons, which are characterized by their unmyelinated axons and which drive hexamethonium-resistant transmission in sympathetic ganglia (McAllen et al, 2005).…”

“…This pathway is thought to activate "accessory" sympathetic preganglionic neurons, which are characterized by their unmyelinated axons and which drive hexamethonium-resistant transmission in sympathetic ganglia (McAllen et al, 2005). Unlike "regular" sympathetic preganglionic neurons, which are inhibited by administration of GABA in the rostral VLM, the "accessory" sympathetic preganglionic neurons are activated by this manipulation (McAllen et al, 2005). Thus, it may be that activation of this "accessory" pathway contributes to resting blood pressure differences between LCR and HCR rats.…”