Evidence for a role of capsaicin-sensitive mucosal afferent nerves in the regulation of mesenteric blood flow in the dog

Multiple impairments of cutaneous nociceptor function induced by cardiotoxic doses of Adriamycin in the rat

“…In addition to the transmission of nociceptive information toward the central nervous system, these primary sensory neurons are involved, through the release of peptides from their peripheral nerve endings, in local regulatory functions of the innervated organs and tissues (Jancsó 1960;Jancsó et al 1968;Jancsó 1984;Jancsó et al 1987;Maggi and Meli 1988;Szolcsányi 1988;Holzer 1998b;Sántha et al 1998;Sántha et al 2000;Nagy et al 2004;Jancsó et al 2009). Of the many facets of these local regulatory functions, sensory neurogenic vasodilatation and plasma extravasation, collectively designated neurogenic inflammation, are particularly important in the modulation of local blood flow, vascular permeability, inflammatory processes, and tissue defense mechanisms (Jancsó 1960;Jancsó et al 1968;Rózsa et al 1986;Maggi et al 1987;Brain 1997;Holzer 1998a;Holzer and Holzer-Petsche 2001;Jancsó et al 2009;Jancsó 2009). A quantitative assessment of the vascular reactions elicited through activation of TRPV1 and/or TRPA1 receptors localized on chemosensitive afferent nerves serves as a reliable indicator of the functional condition of these afferent nerves in both man and animals (Jancsó and Janka 1981;Jancsó et al 1985;Baron et al 1988;Lynn et al 1996;Dux et al 2003;Bernardini et al 2004;Namer et al 2005).…”

Peptidergic sensory neurons in the control of vascular functions: Mechanisms and significance in the cutaneous and splanchnic vascular beds

“…Thus, mesenteric hyperaemia takes place when the sensory neuron stimulant capsaicin is administered into the small intestinal lumen of the dog (R6zsa et al 1986) and rat (R6zsa and Jacobson 1989;Hottenstein et al 1991) or when bile-oleate is given into the rat jejunum (R6zsa and Jacobson 1989). The responses to both capsaicin and bile-oleate are blocked by defunctionalization of capsaicin-sensitive afferent neurons and by local anaesthetics (R6zsa et al 1986;R6sza and Jacobson 1989;Hottenstein et al 1991), which indicates that they are the result of a neural reflex, the precise pathways of which are not known. Mesenteric hyperaemia due to intraluminal bile-oleate remains unaltered by blockade of muscarinic and nicotinic acetylcholine receptors, defunctionalization of noradrenergic neurons with reserpine, or antibodies to cholecystokininoctapeptide and SP (R6sza and Jacobson 1989).…”

“…While a participation of CGRP has not yet been tested, an antibody to VIP has been found to reduce the mesenteric vasodilatation evoked by intraluminal bile-oleate (R6zsa and Jacobson 1989). In delineating the neural pathways of this hyperaemic response, "axon reflexes" have been proposed Io occur between intestinal and mesenteric collaterals of afferent neurons in response to chemical stimulation of afferent nerve endings in the gut (R6zsa et al 1986;R6zsa and Jacobson 1989). This interpretation presupposes that VIP is a dilator transmitter of afferent nerve endings in the rat mesenteric arteries.…”

Ultrastructure of substance P-immunoreactive terminals and their relation to vascular smooth muscle cells of rat small mesenteric arteries

“…These axons may be the collaterals of primary afferent neurones that also project to the intestinal mucosa. It has been suggested that they play a role in an axon reflex that increases intestinal blood flow when chemoreceptors in the gut segment, to which they are also connected, are activated (Rózsa et al, 1986). On the other hand, they may act to signal the central nervous system about the state of the arteries perfusing an individual gut segment (Holzer, 1992).…”