Chronically administered nicotine attenuates bradykinin-induced plasma extravasation and aggravates arthritis-induced joint injury in the rat

Miao, F.J.-P.; Helms, Clyde A.; Benowitz, Neal L.; Basbaum, A. I.; Heller, Philip H.; Levine, Jon D.

doi:10.1016/0306-4522(92)90304-k

Cited by 16 publications

(19 citation statements)

References 15 publications

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“…Although there is no previous disease model in which the CNS is the primary initiator of peripheral inflammation, there is ample evidence of spinally mediated neurogenic inflammation induced by a stimulus to a distant body area (Denko and Petricevic, 1978;Levine et al, 1985a,b;Kolston et al, 1991;Bileviciute et al, 1993;Wesselmann and Lai, 1997). Accordingly, modulation of spinal non-NMDA, GABA-A, A 1 adenosine, or nicotinic receptors reduces peripheral inflammation (Miao et al, 1992;Rees et al, 1994Rees et al, , 1995Rees et al, , 1996Bong et al, 1996). Abnormal activity of spinal interneurons would result in activation of the central branch of primary sensory afferents, leading to increased peripheral release of proinflammatory neuropeptides Rees et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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We present a model of neurogenic cystitis induced by viral infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies virus (PRV) of neuronal populations neighboring those that innervate the bladder consistently led to a localized immune response in the CNS and bladder inflammation. Infection of bladder circuits themselves or of circuits distant from these rarely produced cystitis. Absence of virus in bladder and urine ruled out an infectious cystitis. Total denervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the inflammation. The integrity of central bladder-related circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of noninfected visceral circuits to infected somatic neurons would thus permit a bystander effect, leading to activation of the sensory and autonomic circuits innervating the bladder and resulting in a neurogenic inflammation localized to the bladder. The present study indicates that CNS dysfunction can bring about a peripheral inflammation.

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Section: Discussionmentioning

confidence: 99%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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“…Inhibition of rat knee joint plasma extravasation is associated with worsening of joint injury in experimental arthritis (14)(15)(16). Plasma extravasation may exert a protective effect by increasing extravasation of plasma proteinase inhibitors (e.g., ␣ 1 -proteinase inhibitor, ␣ 1 -anti-chymotrypsin, and ␣ 2 -macroglobulin) that control excessive proteolytic activity and thereby protect against connective tissue damage (26), or by increasing the rate of removal of tissue-injurious products of the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Repeated, but not acute, stress suppresses inflammatory plasma extravasation

Strausbaugh

Dallman

Levine

1999

Proc. Natl. Acad. Sci. U.S.A.

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Clinical findings suggest that inflammatory disease symptoms are aggravated by ongoing, repeated stress, but not by acute stress. We hypothesized that, compared with single acute stressors, chronic repeated stress may engage different physiological mechanisms that exert qualitatively different effects on the inflammatory response. Because inhibition of plasma extravasation, a critical component of the inflammatory response, has been associated with increased disease severity in experimental arthritis, we tested for a potential repeated stress-induced inhibition of plasma extravasation. Repeated, but not single, exposures to restraint stress produced a profound inhibition of bradykinin-induced synovial plasma extravasation in the rat. Experiments examining the mechanism of inhibition showed that the effect of repeated stress was blocked by adrenalectomy, but not by adrenal medullae denervation, suggesting that the adrenal cortex mediates this effect. Consistent with known effects of stress and with mediation by the adrenal cortex, restraint stress evoked repeated transient elevations of plasma corticosterone levels. This elevated corticosterone was necessary and sufficient to produce inhibition of plasma extravasation because the stress-induced inhibition was blocked by preventing corticosterone synthesis and, conversely, induction of repeated transient elevations in plasma corticosterone levels mimicked the effects of repeated stress. These data suggest that repetition of a mild stressor can induce changes in the physiological state of the animal that enable a previously innocuous stressor to inhibit the inflammatory response. These findings provide a potential explanation for the clinical association between repeated stress and aggravation of inflammatory disease symptoms and provide a model for study of the biological mechanisms underlying the stress-induced aggravation of chronic inflammatory diseases. There is considerable evidence that stress can exacerbate a number of chronic inflammatory diseases. For example, repeated mild daily stressors have been associated with exacerbation of rheumatoid arthritis (1, 2), ulcerative colitis (3), inflammatory bowel disease (4), and asthma (5). Patients with rheumatoid arthritis (6) cite stress as the most frequent antecedent of symptom flares, and stress management interventions can reduce symptoms (7). Similarly, studies in animal models of arthritis (8, 9) demonstrate that stress can exacerbate disease activity. Very little is known, however, about the biological mechanisms by which stress may exert these effects.Acute stress (10, 11), as well as acute activation of neuroendocrine circuits known to be activated by stressful stimuli (12, 13), transiently suppresses the inflammatory response. However, exacerbation of inflammatory diseases has been correlated with chronic repeated exposure to stressful stimuli rather than with exposure to a single acute stressor (2-4). We hypothesized that, compared with single acute stressors, chronic repeated stress may engage differe...

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“…To remove adrenal medullas, the adrenal glands were located in ether-anesthetized rats through an incision in the lateral abdominal wall. The capsule of the gland was cut open, and the adrenal medulla was removed (Wilkinson et al, 1981;Miao et al, 1992). Rats were given 0.5% saline to drink in place of water for the first 7 d after surgery.…”

Section: Methodsmentioning

confidence: 99%

Vagotomy-Induced Enhancement of Mechanical Hyperalgesia in the Rat Is Sympathoadrenal-Mediated

et al. 1998

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We have recently shown that subdiaphragmatic vagotomy enhances bradykinin-induced hyperalgesic behavior and decreases baseline paw withdrawal threshold to mechanical stimulation of the hindpaw skin in rats by a peripheral mechanism. To elucidate the underlying mechanism, we studied whether lesions of efferent neuroendocrine pathways could prevent or reverse the potentiating effect of vagotomy. In groups of shamvagotomized or vagotomized rats, we surgically removed or denervated the adrenal medulla. Bradykinin was injected intradermally into the skin of the dorsal surface of the rat hindpaw. Threshold of paw withdrawal to mechanical stimulation of the skin was measured.Vagotomy induced a decrease in mechanical baseline paw withdrawal threshold and enhancement of bradykinin-induced mechanical hyperalgesic behavior, both of which were maintained over the 5 week testing period. Adrenal enucleation or denervation of the adrenal gland by suprarenal ganglionectomy prevented vagotomy-induced decrease in baseline paw withdrawal threshold and enhancement of bradykinin-induced hyperalgesia. In animals that had a demonstrated decrease in baseline paw withdrawal threshold and enhancement of bradykinin-induced hyperalgesia 2 weeks after vagotomy, additional denervation of the adrenal medulla significantly reversed these effects over a 3 week period.These results imply that both the decrease in baseline paw withdrawal threshold and enhancement of bradykinin-induced hyperalgesic behavior after vagotomy are dependent on a hormonal signal released from the adrenal medulla and suggest a novel mechanism of sensitization of cutaneous nociceptors. Key words: bradykinin; hyperalgesia; nociception; pain; sympathoadrenal system; vagusIn the rat, activity in vagal afferents from abdominal organs modulates transmission of nociceptive impulses in the spinal cord and probably elsewhere in the C NS and also affects experimental pain behavior Randich and Gebhart, 1992; Watkins and Maier, 1995a,b). Recently, we have shown that bradykinin (BK)-induced mechanical cutaneous hyperalgesia is significantly enhanced after subdiaphragmatic vagotomy. A similar effect was seen after cutting the celiac branches of the abdominal vagus nerve but not after cutting only its gastric and hepatic branches. Furthermore, baseline mechanical paw withdrawal threshold decreased after vagotomy. The enhanced mechanical hyperalgesia produced by subdiaphragmatic vagotomy was specific for hyperalgesia induced by BK . Hyperalgesia induced by the direct-acting hyperalgesic agent prostaglandin E 2 (PGE 2 ) was not affected by vagotomy (K hasar et al., 1997). These findings argue that enhancement of BK-induced mechanical hyperalgesia and decrease in baseline mechanical paw withdrawal threshold after abdominal vagotomy are produced by a peripheral mechanism. However, as the experimental results reported in this manuscript show, we do not exclude a central component in enhancement of BK-induced hyperalgesia after vagotomy, as predicted by the work of Gebhart and Randich (1992)...

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Chronically administered nicotine attenuates bradykinin-induced plasma extravasation and aggravates arthritis-induced joint injury in the rat

Cited by 16 publications

References 15 publications

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

Repeated, but not acute, stress suppresses inflammatory plasma extravasation

Vagotomy-Induced Enhancement of Mechanical Hyperalgesia in the Rat Is Sympathoadrenal-Mediated

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