Prostacyclin activates tachykinin release from capsaicin‐sensitive afferents in guinea‐pig bronchi through a ruthenium red‐sensitive pathway

Mapp, C. E.; Fabbri, Leonardo; Boniotti, Anna; Maggi, Carlo Alberto

doi:10.1111/j.1476-5381.1991.tb12383.x

Cited by 39 publications

(18 citation statements)

References 21 publications

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“…In contrast, both bradykinin and prostanoids have been shown to evoke neuropeptide release from sensory nerve terminals in various peripheral tissues (Amann et al, 1989;Franco-Cereceda et al, 1989;Geppetti et al, 1990a,b;1991;Mapp et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Effect of bradykinin and prostaglandins on the release of calcitonin gene‐related peptide‐like immunoreactivity from the rat spinal cord in vitro

Andreeva

Rang²

1993

British J Pharmacology

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1 The release of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) from the dorsal horn of the rat spinal cord in vitro in response to dorsal root stimulation was measured by radioimmunoassay.2 Stimulation of the dorsal roots (3 or 4 roots on each side) at 10 Hz for 5 min evoked a mean release (RI) of 134.3 ± 17.5 (n = 10) fmol CGRP-LI; the release (R2) evoked by a second stimulation period 30 min later under control conditions was 77 ± 10% (n = 10) of RI. Test compounds were applied to the preparation following release RI, and their effect calculated from the value of R2/R,. 3 Bradykinin (0.01-10 pM) had no significant effect on the basal release of CGRP-LI, but at 0.1-10MM it increased 2-3 fold the release evoked by dorsal root stimulation.4 This effect of bradykinin was prevented by indomethacin (10 pM), or by the B2-receptor antagonist, Hoel40 (1-1I0 M). In the presence of Hoel40, bradykinin significantly reduced R2/R,; the explanation for this is not clear.5 The B,-receptor agonist, Des-Arg-bradykinin (1OMM), did not affect CGRP-LI release nor was the effect of bradykinin blocked by the B,-receptor antagonist, Des-Arg9-Leu8-bradykinin (10MM). 6 Various prostaglandins were found to mimic the effect of bradykinin on CGRP-LI release. Their approximate order of potency was prostaglandin D2 (PGD2) = PGE, > PGF2. = PGE2; PGI2 was ineffective at 1O MM.7 Forskolin (30 MM) and 3-isobutyl l-methylxanthine (IBMX; 10 fM) also increased the evoked release of CGRP-LI. 8 It is concluded that bradykinin acts on B2-receptors in the spinal cord, causing the formation of prostanoids, which in turn cause an enhancement of neuropeptide release from primary afferent nerve terminals in the dorsal horn. This effect may be secondary to activation of adenylate cyclase. Because B2-receptors are mainly associated with primary afferent nerve terminals, it is likely that prostanoid production is also a function of these structures. Whether this action of bradykinin has any physiological function in nociceptive transmission remains unclear.

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Section: Discussionmentioning

confidence: 99%

Effect of bradykinin and prostaglandins on the release of calcitonin gene‐related peptide‐like immunoreactivity from the rat spinal cord in vitro

Andreeva

Rang²

1993

British J Pharmacology

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“…For instance, in the atrioventricular fistula model of heart failure, there are increased levels of PGI2 in the pericardial effusate.39 Since the model we used has been characterized histologically as being consistent with chronic ischemia,40 there may be several substances that are released by the myocardium that potentiate the response to PGI2, such as potassium and bradykinin 35,41. In an important study byMapp et al,42 it was shown that the ability of PGI2 to contract guinea pig isolated bronchi was mediated by capsaicin-sensitive afferents. A selective inhibitor of NK-2-tachykinin receptors decreased the PGI2 contractions.…”

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confidence: 97%

Ventricular mechanoreflex and chemoreflex alterations in chronic heart failure.

Brändle¹,

Wang²,

Zucker³

1994

Circulation Research

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Cardiac and arterial baroreflex control of the circulation is abnormal in both human and experimental heart failure. Ventricular vagal afferents mediate mechanical and chemical reflexes, which result in bradycardia and hypotension. The aim of the present study was to evaluate the changes that occur in ventricular mechanoreflexes and chemoreflexes in a conscious canine model of chronic heart failure. Dogs were instrumented for the measurement of left ventricular pressure, left atrial pressure, arterial pressure, and heart rate. Vascular occluders were placed on the ascending thoracic aorta, on the descending thoracic aorta, and on the thoracic inferior vena cava. A chronic left circumflex coronary artery catheter was also implanted. Finally, a pacing lead was secured to the left ventricular free wall. After recovery from surgery (10 to 14 days), the dogs were subjected to complete arterial baroreceptor denervation. The responses to vascular occlusions and intracoronary administration of prostacyclin (PGI2) were carried out before and after heart failure was induced by chronic cardiac pacing at 250 beats per minute. PGI2 was used as a chemical stimulus for ventricular afferents; ascending aortic occlusion was used as a mechanical stimulus. Before chronic pacing, ascending aortic occlusion resulted in a decrease in heart rate of 36.1 +/- 12.3 beats per minute (mean +/- SD, P < .001). After heart failure was induced, the heart rate response to ascending aortic occlusion was almost completely abolished. The slope of the linear relation between pulse interval and left ventricular end-diastolic pressure was reduced by 90.5% from a control value of 11.3 +/- 6.9 ms/mm Hg after heart failure had been induced.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Therefore, endogenous prostaglandins may potentiate the response of asthmatic airway nerves to inhaled NKA, and only part of the effects of NKA may result from the direct release of contractile prostaglandins. On the other hand, cyclooxygenase products activate tachykinin release from capsaicin-sensitive afferents in guinea-pig airways [33], and stimulate both pulmonary and bronchial C fibres in dogs [34]. Other possible explanations for the L-ASA reduction in NKA responsiveness in asthma may include down regulation of NK receptors, and modulation of postreceptor events coupled to NKA-mediated contraction of smooth muscle.…”

Section: Discussionmentioning

confidence: 99%

Changes in neurokinin A airway responsiveness with inhaled lysine-acetylsalicylate in asthma

Crimi

Polosa²,

Prosperini³

et al. 1996

Eur Respir J

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The small decrease in airway responsiveness to neurokinin A after administration of lysine acetylsalicylate by inhalation suggests that endogenous prostaglandins may play a contributory protective role in the airway response to neurokinin A in human asthma. Eur Respir J., 1996Respir J., , 9, 1139Respir J., -1145 Sensory neuropeptides, such as substance P (SP) and neurokinin A (NKA), exhibit a range of features which may be relevant to the pathophysiology of asthma, including contraction of airway smooth muscle, increased vascular permeability, mucus secretion and activation of cholinergic neurotransmission [1]. Immunocytochemical studies have demonstrated the presence of sensory neuropeptides and their receptors within the upper and lower airways both in man and rodents [2][3][4]. Although compared with rodents the nerve fibres containing sensory neuropeptides are less dense in human airway tissue, recent studies on necroscopic tissue, bronchoalveolar lavage fluid, and induced sputum have shown increased amounts of SP in the airways of asthmatics compared to controls [5][6][7]. Different authors have demonstrated that both SP and NKA produce dose-related bronchoconstriction when administered by inhalation to asthmatic subjects, NKA being more potent than SP and asthmatic subjects being more responsive than normal subjects [8][9][10][11][12].The mode of action by which sensory neuropeptides elicit bronchoconstriction in asthma is not well understood. The bronchoconstrictor effect of nebulized NKA in asthmatic patients is inhibited by prior treatment with nedocromil sodium [10,13], suggesting that this response may be evoked indirectly rather than through direct stimulation of airway smooth muscle. There is some support for an action of sensory neuropeptides in eliciting prostaglandin synthesis. Recent in vitro studies support the view that many of the biological responses of the sensory neuropeptides may result from the local release of bioactive prostanoids [14][15][16].In line with the notion that administration of bronchoactive drugs by inhalation achieves maximum effect with smaller doses, BIANCO and co-workers [17,18] have recently shown that the potent cyclooxygenase inhibitor, aspirin administered as an aerosol of lysine acetylsalicylate (L-ASA) solution elicits better protection against nonspecific stimuli in the airways of asthmatics than when given orally. Using this alternative experimental approach, we intend to expand our previous observations with other nonspecific agonists [19,20], by evaluating the relative contribution of contractile prostaglandins to the airway response provoked by inhaled NKA in asthmatic subjects.

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Prostacyclin activates tachykinin release from capsaicin‐sensitive afferents in guinea‐pig bronchi through a ruthenium red‐sensitive pathway

Cited by 39 publications

References 21 publications

Effect of bradykinin and prostaglandins on the release of calcitonin gene‐related peptide‐like immunoreactivity from the rat spinal cord in vitro

Effect of bradykinin and prostaglandins on the release of calcitonin gene‐related peptide‐like immunoreactivity from the rat spinal cord in vitro

Ventricular mechanoreflex and chemoreflex alterations in chronic heart failure.

Changes in neurokinin A airway responsiveness with inhaled lysine-acetylsalicylate in asthma

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