Enhancement by Parainfluenza 3 Infection of Contractile Responses to Substance P and Capsaicin in Airway Smooth Muscle from the Guinea Pig

Saban, Ricardo; Dick, Elliot C.; Fishleder, R I; Buckner, Carl K.

doi:10.1164/ajrccm/136.3.586

Cited by 89 publications

(26 citation statements)

References 19 publications

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“…Airway contractions in response to substance P and capsaicin are increased in Virus-induced Airway Hyperresponsiveness and Nitric Oxide PI-3 virus-infected guinea pigs (34). Further, as shown by Jacoby et al (35), the enzymatic activity of enkephalinase is decreased and the reactivity to substance P is increased in ferret airways tissues incubated with influenza virus for 4 d. Further, we showed that the anti-tussive drug levodropropizine could prevent the development of the virus-induced airway hyperresponsiveness (36).…”

Section: Discussionmentioning

confidence: 96%

Virus-induced airway hyperresponsiveness in guinea pigs is related to a deficiency in nitric oxide.

Folkerts¹,

Linde²,

Nijkamp³

1995

J. Clin. Invest.

103

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Intratracheal inoculation of parainfluenza type 3 virus to guinea pigs induces a marked increase in airway responsiveness in vivo and in vitro. In spontaneously breathing anesthetized guinea pigs inhalation of an aerosol containing the nitric oxide (NO) precursor L-argimine (2.0 mM) completely prevented the virus-induced airway hyperresponsiveness to histamine. In addition, perfusion of L-arginine (200 pAM) or the direct NO-donor S-nitroso-N-acetyl-penicillamine (SNAP, 1 ,uM) through the lumen of tracheal tubes from infected animals prevented the increase in airway responsiveness to histamine or the cholinoceptor agonist methacholine. The NO synthase inhibitor Na-nitro-Larginine methyl ester (L-NAME, 120 ,uM) did not further increase the virus-induced airway hyperresponsiveness.In An NO deficiency might be causally related to the development of airway hyperresponsiveness after a viral respiratory infection. (J. Clin. Invest. 1995. 95:26-30.)

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Section: Discussionmentioning

confidence: 96%

Virus-induced airway hyperresponsiveness in guinea pigs is related to a deficiency in nitric oxide.

Folkerts¹,

Linde²,

Nijkamp³

1995

J. Clin. Invest.

103

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“…It is then likely that airway epithelial damage can increase the responsiveness to various inhaled irritants via an impairment of the NEP-like activity. Support for this reasoning is given by studies showing that viral infections enhance the contractile responses to SP in guinea-pig bronchi (Saban et al, 1987) and ferret trachea (Jacoby et al, 1988). Furthermore, histories of infections in rats have been associated with a decreased activity of NEP and an enhanced SP-induced vascular leakage in the trachea (Borson et al, 1989).…”

Section: Discussionmentioning

confidence: 97%

Effects of aerosolised substance P on lung resistance in guinea‐pigs: a comparison between inhibition of neutral endopeptidase and angiotensin‐converting enzyme

Lötvall

Skoogh

Barnes

et al. 1990

British J Pharmacology

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1We have examined in guinea-pigs, in vivo, the effects of inhibition of neutral endopeptidase (NEP) and angiotensin-converting enzyme (ACE) on the airway response to aerosolised substance P (SP). We aerosolised captopril (4.6mM, 60 breaths; 210nmol) to inhibit ACE and acetorphan (0.3, 1 and 3mM, 60 breaths; 9nmol, 33nmol and 110nmol respectively) to inhibit NEP. We also examined the effect of the highest dose of acetorphan (110 nmol) on the response to aerosolised acetylcholine (ACh).2 Responsiveness to SP (or ACh) was measured as the change in lung resistance (RL) induced by nebulisation of increasing concentrations of SP (or ACh) before and after treatment with the inhibitor. PC200, defined as the provocative concentration inducing an increase in RL of 200% above baseline, was calculated for each challenge. 3 Administration of acetorphan before the second SP-challenge induced a dose-dependent decrease in PC200 for SP amounting to 1.8 (± 0.3) log units after treatment with 11 nmol acetorphan. Treatment with vehicle before the second SP-challenge or with 3 mM acetorphan before the second ACh-challenge had no significant effect on PC200. 4 Treatment with captopril (21 nmol) induced only a small, nonsignificant leftward shift of PC200 to SP (0.3 + 0.2 log units). 5 We conclude that a NEP-like enzyme, but not ACE, regulates the response to aerosolised SP. We suggest that the same is true for SP released endogenously from sensory nerve endings in the airway epithelial layer.

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“…Infections with Mycoplasma pulmonis can produce a 30-fold increase in the magnitude of neurogenic plasma extravasion in rat airways (Figure 3) (77). Similarly, respiratory infections of rodents with Sendai virus (parainfluenza type 1) can potentiate substance P-induced increases in airways blood flow (78) and enhance tachykinergic nerve-mediated contraction of airway smooth muscle (79). These effects appear to be at least partially due to decreased activity of neutral endopeptidase, a protease normally present in the airways, which degrades tachykinins (80)(81)(82).…”

Section: Enhanced Release Of Tachykininsmentioning

confidence: 99%

Inflammation-Induced Plasticity of the Afferent Innervation of the Airways

Carr¹,

Undem²

2001

Environmental Health Perspectives

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Enhancement by Parainfluenza 3 Infection of Contractile Responses to Substance P and Capsaicin in Airway Smooth Muscle from the Guinea Pig

Cited by 89 publications

References 19 publications

Virus-induced airway hyperresponsiveness in guinea pigs is related to a deficiency in nitric oxide.

Virus-induced airway hyperresponsiveness in guinea pigs is related to a deficiency in nitric oxide.

Effects of aerosolised substance P on lung resistance in guinea‐pigs: a comparison between inhibition of neutral endopeptidase and angiotensin‐converting enzyme

Inflammation-Induced Plasticity of the Afferent Innervation of the Airways

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