Adenosine Enhances the Bronchocontractile Response to Histamine in Anaesthetized and Curarized Guinea Pigs through a Mechanism Partly Blocked by Hexamethonium

Breschi, Maria Cristina; Nieri, Paola; Lazzeri, Nicola; Martinotti, Enrica

doi:10.1159/000139215

Cited by 11 publications

(10 citation statements)

References 29 publications

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“…tachykinergic) excitatory system, adenosine has been found to reduce the EFS-induced substance-P-mediated contraction in the guinea pig airways through the activation of prejunctional A 1 and A 2 receptors [41]. By contrast, another study questioned any involvement of adenosine in the modulation of the noncholinergic excitatory system in the airways of the same species [51]. …”

Section: Discussionmentioning

confidence: 99%

Adenosine A1 and A3 Receptor Agonists Inhibit Nonadrenergic, Noncholinergic Relaxations in the Guinea Pig Isolated Trachea

Dellabianca¹,

Faniglione²,

Angelis³

et al. 2008

Respiration

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Background: Adenosine affects the tone and reactivity of airways by activating specific membrane receptors, named A₁, A_2a, A_2b and A₃. It affects cellular activities either directly by regulating membrane ion exchanges and polarization, or indirectly by modifying neurotransmitter release. Objectives: We assessed the effect of A₁ and A₃ receptor activation on electrically induced nonadrenergic, noncholinergic (NANC) relaxations in the guinea pig isolated trachea and the localization of A₁ and A₃ receptors in tracheal inhibitory neurons. Methods: NANC responses at 3 Hz were evaluat- ed in the presence of 2-chloro-N⁶-cyclopentyladenosine (CCPA), a selective A₁ agonist, and 2-chloro-N⁶-(3-iodobenzyl)-adenosine-5′-N-methyluronamide (Cl-IB-MECA), a selective A₃ agonist, before and after the administration of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective A₁ antagonist, or 9-chloro-2-(2-furanyl)-5-((phenylacetyl)amino[1,2,4]triazolo[1,5-c])quinazoline (MRS 1220), a selective A₃ antagonist, respectively. For immunohistochemistry, tissues were exposed to antibodies to HuC/D, a general neuronal marker, neuronal nitric oxide synthase (nNOS), and A₁ or A₃ adenosine receptors and processed by indirect immunofluorescence. Results: CCPA (10 nM–3 μM) inhibited NANC relaxations. DPCPX (10 nM) failed to antagonize the effect of CCPA, but inhibited per se NANC relaxations (range 0.1–100 nM). CCPA (10 nM–10 μM) contracted unstimulated tracheal preparations, an effect antagonized by 10 nM DPCPX, with a pK_B value of 8.43. Cl-IB-MECA (10 nM–3 μM) inhibited NANC relaxations through a mechanism antagonized by MRS 1220 (100 nM). A₁- and A₃-positive neurons containing nNOS were detected in tracheal sections. Conclusions: Enogenous adenosine may induce airway hyperresponsiveness by inhibiting NANC relaxations via A₁ and A₃ receptors.

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Section: Discussionmentioning

confidence: 99%

Adenosine A1 and A3 Receptor Agonists Inhibit Nonadrenergic, Noncholinergic Relaxations in the Guinea Pig Isolated Trachea

Dellabianca¹,

Faniglione²,

Angelis³

et al. 2008

Respiration

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“…* P ≤ 0.05; ** P ≤ 0.01. [Breschi et al, 1994], allowed us to test the influence of theophylline on the potentiating activity of adenosine versus a dose of histamine similar to that used in control experiments.…”

Section: Discussionmentioning

confidence: 99%

“…Also in our laboratory, an animal model has been described, in which the nucleoside, although not able to induce bronchospasm per se, enhances the bronchial responsiveness to histamine by means of a neuralmediated action [Breschi et al, 1994] in addition to a mechanism involving the release of lipoxygenase products [Nieri et al, 1997]. A bronchial hyperresponsiveness to histamine after exposure to adenosine has been reported also in allergic rabbit by Ali et al [1994].…”

Section: Introductionmentioning

confidence: 93%

“…So, we reevaluated in the presence of propranolol the influence of theophylline on the adenosine potentiation because propranolol per se did not alter the effect of the nucleoside [Breschi et al, 1994]. Also in this case, the effect of theophylline was a complete inhibition of the potentiating effect of adenosine, as observed in the absence of propranolol (response to histamine,115.3 ± 8.2% of control, n = 4).…”

Section: Antagonistsmentioning

confidence: 98%

“…

ABSTRACTA potentiating effect by adenosine on the bronchocontractile response to histamine has been previously described in a guinea-pig model (Breschi et al [1994] Pharmacology 49:42-51). In the present study, the subtype(s) of purinergic receptors involved in this modulatory effect of the nucleoside have been investigated.

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confidence: 90%

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Potentiation by adenosine of histamine-induced bronchospasm in anaesthetized guinea-pig: Receptor subtype/s involved

Breschi¹,

Nieri

Lazzeri

et al. 1998

Drug Dev. Res.

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ATP causes neurogenic bronchoconstriction in the dog

Katchanov¹,

Schulman²,

Pelleg³

1998

Drug Dev. Res.

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Adenosine 5′‐triphosphate (ATP) causes bronchoconstriction in normal and asthmatic human subjects. The mechanism of this action is not known. Because ATP is known to elicit vagal afferent neural traffic by stimulating pulmonary vagal C‐fiber terminals, we have hypothesized that this action of ATP results in reflex bronchoconstriction. To test this hypothesis, ATP, adenosine, and capsaicin were administered as rapid boluses into the right atrium of anesthetized dogs (n = 8) before and after either atropine or bilateral cervical vagotomy. ATP and adenosine were given also in the presence of physostigmine to accentuate vagal input into the lungs. Fluoroscopic visualization of the bronchial tree was achieved by insufflation of heavy metal powder into the lungs. Bronchi diameters were determined using bronchograms. Pulmonary dynamics were quantitated using tracheal and esophageal pressures and respiratory air flow. ATP, adenosine, and capsaicin caused bronchoconstriction that was eliminated by either atropine or vagotomy. The effect of ATP was much more pronounced (P < 0.05) than that of adenosine and capsaicin: the diameter of generation III bronchi of 6.8 ± 0.8 mm was reduced by 27.5 ± 2.1%, 10.0 ± 2.1%, and 15.4 ± 3.3% by ATP, adenosine, and capsaicin, respectively. Similarly, in the presence of physostigmine, lung resistance of 2.67 ± 0.24 mmH2O/l per min and 2.76 ± 0.20 was increase by 68 ± 25% and 16 ± 12% by ATP and adenosine, respectively (P < 0.05). Because endogenous ATP is released into the extracellular space under physiologic and pathophysiologic conditions, the present data indicated that endogenous ATP could trigger neurogenic bronchoconstriction and thereby play a mechanistic role in obstructive airway diseases in general and asthma in particular. Drug Dev. Res. 45:342–349, 1998. © 1998 Wiley‐Liss, Inc.

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Adenosine Enhances the Bronchocontractile Response to Histamine in Anaesthetized and Curarized Guinea Pigs through a Mechanism Partly Blocked by Hexamethonium

Cited by 11 publications

References 29 publications

Adenosine A<sub>1</sub> and A<sub>3</sub> Receptor Agonists Inhibit Nonadrenergic, Noncholinergic Relaxations in the Guinea Pig Isolated Trachea

Adenosine A<sub>1</sub> and A<sub>3</sub> Receptor Agonists Inhibit Nonadrenergic, Noncholinergic Relaxations in the Guinea Pig Isolated Trachea

Potentiation by adenosine of histamine-induced bronchospasm in anaesthetized guinea-pig: Receptor subtype/s involved

ATP causes neurogenic bronchoconstriction in the dog

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