Search results for "Free nerve ending"
showing 4 items of 4 documents
Inactivation and tachyphylaxis of heat-evoked inward currents in nociceptive primary sensory neurones of rats.
2000
In contrast to other sensory modalities, pain does not decrease when a noxious stimulus is applied at constant intensity (Greene & Hardy, 1962). From this lack of adaptation on the perceptive level it has traditionally been implied that primary nociceptive afferents also do not adapt upon constant stimulation. This is in contrast to the results of recordings from these afferents, which exhibit pronounced adaptation for physical as well as chemical stimuli (Meyer et al. 1994). Peripheral adaptation of nociceptive nerve endings is compensated by central summation (Mendell & Wall, 1965; Price et al. 1977); this slow summation process of small fibre input to the dorsal horn of the spinal cord i…
Nitric oxide-mediated beta 2-adrenoceptor relaxation is impaired in mesenteric veins from portal-hypertensive rats.
1996
Abstract BACKGROUND & AIMS: beta-Adrenergic relaxation seems to be mediated by nitric oxide. The aim of this study was to evaluate changes induced by portal hypertension in beta 2-adrenergic vasorelaxation. METHODS: Isolated rat mesenteric veins were relaxed by salbutamol, and nerve- mediated vasocontractions were induced by electrical field stimulation. Responses were evaluated in the presence of NG-nitro-L-arginine methyl ester (L-NAME) or tetrodotoxin. Immunocytochemical techniques were used for localization of neuronal NO synthase. RESULTS: Salbutamol-induced relaxations were decreased in rings from portal-hypertensive animals. L- NAME reduced these relaxations, but its effects were mor…
Opioid-Sensitive Peripheral Neuronal Activity in the Modulation of Gastric Mucosal Injury
1991
There is growing evidence that capsaicin-sensitive afferent neurones participate in the protective mechanisms of the gastric mucosa against damage. Animals pretreated systemically with capsaicin, at doses that lead to the ablation of capsaicin-sensitive afferent neurons, show an increase in the level of macro-scopically apparent mucosal damage in different experimental models of ulceration (Szolcsanyi and Bartho, 1981; Holzer and Sametz, 1986). Furthermore, acute stimulation with capsaicin of afferent nerve endings located in the gastric mucosa protects against different ulcerogenic mechanisms (Szolcsanyi and Bartho, 1981; Holzer and Lippe, 1988; Holzer et al., 1989).