scholarly journals Role of nitric oxide and septide-insensitive NK1 receptors in bronchoconstriction induced by aerosolised neurokinin A in guinea-pigs

2000 ◽  
Vol 129 (5) ◽  
pp. 915-920 ◽  
Author(s):  
Fabio L M Ricciardolo ◽  
Marcello Trevisani ◽  
Pierangelo Geppetti ◽  
Jay A Nadel ◽  
Silvia Amadesi ◽  
...  
2001 ◽  
Vol 90 (4) ◽  
pp. 1474-1480 ◽  
Author(s):  
Oscar E. Suman ◽  
Kenneth C. Beck

Airway function is largely preserved during exercise or isocapnic hyperventilation in humans and guinea pigs despite likely changes in airway milieu during hyperpnea. It is only on cessation of a hyperpneic challenge that airway function deteriorates significantly. We tested the hypothesis that nitric oxide, a known bronchodilator that is produced in the lungs and bronchi, might be responsible for the relative bronchodilation observed during hyperventilation (HV) in guinea pigs. Three groups of anesthetized guinea pigs were given saline and three groups given 50 mg/kg N G-monomethyl-l-arginine (l-NMMA), a potent nitric oxide synthase inhibitor. Three isocapnic ventilation groups included normal ventilation [40 breaths/min, 6 ml/kg tidal volume (Vt)], increased respiratory rate only (150 breaths/min, 6 ml/kg Vt), and increased respiratory rate and increased volume (100 breaths/min, 8 ml/kg Vt). l-NMMA reduced expired nitric oxide in all groups. Expired nitric oxide was slightly but significantly increased by HV in the saline groups. However, inhibition of nitric oxide production had no significant effect on rate of rise of respiratory system resistance (Rrs) during HV or on the larger rise in Rrs seen 6 min after HV. We conclude that nitric oxide synthase inhibition has no effect on changes in Rrs, either during or after HV in guinea pigs.


1998 ◽  
Vol 123 (7) ◽  
pp. 1450-1456 ◽  
Author(s):  
Martin Schuiling ◽  
Annet B. Zuidhof ◽  
Monique A. A. Bonouvrie ◽  
Nicolette Venema ◽  
Johan Zaagsma ◽  
...  

1999 ◽  
Vol 84 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Sedat Altuǧ ◽  
Özge Uzun ◽  
A. Tuncay Demiryürek ◽  
İclal Çakıcı ◽  
Nurettin Abacıoǧlu ◽  
...  
Keyword(s):  

2010 ◽  
Vol 36 (2) ◽  
pp. 67-74 ◽  
Author(s):  
Patrícia Pennacchioni-Alves ◽  
Rodolfo Paula Vieira ◽  
Fernanda Degobi Tenório Quirino Santos Lopes ◽  
Fernanda Magalhaes Arantes-Costa ◽  
Fabia B. Pianheri ◽  
...  

1998 ◽  
Vol 274 (3) ◽  
pp. G480-G486
Author(s):  
Per M. Hellström ◽  
Mikael Thollander ◽  
Elvar Theodorsson

This study investigated the role of nitric oxide (NO) and adrenergic and dopaminergic mechanisms in reflex inhibition of the migrating myoelectric complex (MMC) after intraperitoneal administration of acid in rats. Acid instilled immediately after an activity front inhibited the migrating complex and prolonged the cycle length from 13.0 ± 0.7 to 98.5 ± 17.2 min ( P < 0.001). Administration of Nω-nitro-l-arginine, reserpine, or guanetidine before acid decreased the prolonged cycle length to 18.1 ± 2.8 ( P < 0.001), 19.0 ± 2.0 ( P < 0.001), and 27.5 ± 9.3 min ( P < 0.001), respectively. Similarly, haloperidol given before acid shortened the prolonged cycle length to 46.7 ± 5.2 min ( P < 0.05). There was no effect of phentolamine in combination with propranolol or hexamethonium given alone. After intraperitoneal instillation of acid there was an increase in the plasma levels of somatostatin and a decrease of calcitonin gene-related peptide, but there was no change of neuropeptide Y, vasoactive intestinal peptide, substance P, neurokinin A, or neurotensin. The results indicate that NO and adrenergic, dopaminergic, and somatostatinergic mechanisms cooperate in inhibiting the MMC after nociceptive stimulation of the peritoneum.


2001 ◽  
Vol 133 (8) ◽  
pp. 1235-1242 ◽  
Author(s):  
Jacob de Boer ◽  
Herman Meurs ◽  
Leonard Flendrig ◽  
Miranda Koopal ◽  
Johan Zaagsma

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