vasoactive-intestinal-peptide and Bronchial-Spasm

Topics: Adrenergic beta-Agonists; Asthma; Atrial Natriuretic Factor; Bronchial Spasm; Bronchodilator Agents; Humans; Ion Channels; Muscle Relaxation; Muscle, Smooth; Phosphodiesterase Inhibitors; Respiratory Muscles; Vasoactive Intestinal Peptide

There is now considerable evidence in favor of vasoactive intestinal peptide (VIP) as a neurotransmitter of nonadrenergic noncholinergic nerves in the airways. The purpose of our study was to evaluate the influence of inhaled VIP on bronchomotor tone after a beta-adrenergic- and cholinergic-receptor blockage. The study was performed in six patients with asthma in 4 days. On the first day, a propranolol provocative dose producing a 20% change in FEV1 (PD20) was determined from the individual semilogarithmic dose-response curve. On the other days, the propranolol challenge was performed after inhalation of ipratropium bromide (40 micrograms), VIP (70 micrograms), and both drugs in randomized double-blind order. Statistical analysis was performed by two-way analysis of variance. The results demonstrated that mean propranolol PD20 was 0.14 mg (geometric mean + SD = 1.22). Ipratropium bromide administration, like VIP administration, significantly raised the PD20 value. The administration of both drugs elicited a further remarkable increase of mean propranolol PD20. The results demonstrated that inhaled VIP influences bronchomotor tone and that this effect is independent of the cholinergic blockage.

Topics: Adult; Aerosols; Asthma; Bronchial Provocation Tests; Bronchial Spasm; Bronchodilator Agents; Female; Forced Expiratory Volume; Humans; Ipratropium; Male; Propranolol; Vasoactive Intestinal Peptide

In anaesthetized guinea pigs, adenosine enhances the histamine-induced bronchospasm by means of a mechanism partly involving non-adrenergic-non-cholinergic (NANC) nerves, not related to capsaicin-sensitive neurons (Breschi et al., 1994). In the present paper, we excluded any interference by adenosine with the mediators known to be present in the airway inhibitory NANC system, VIP (vasoactive intestinal polypeptide) and NO (nitric oxide). The use of alpha-chymotrypsin or L-N(G)-nitro-arginine methyl ester (L-NAME) failed to modify the potentiation under study. The effects of adenosine were further investigated by studying whether an increased release of excitatory mediators from non-neural cells, in particular 5-HT (5-hydroxytryptamine, serotonin) and arachidonic products, was involved. In this connection, methysergide did not significantly affect the modulatory action of adenosine, revealing that the release of 5-HT was also not involved. Inhibition was obtained with hydrocortisone and with nordihydroguaiaretic acid, but not with indomethacin or with the mastocyte membrane stabilizer, sodium cromoglycate. This evidence suggests that lipooxygenase products, not derived from mastocytes, probably participate in the potentiating effect of adenosine.

Topics: Adenosine; Animals; Arachidonic Acids; Autonomic Nervous System; Bronchial Spasm; Down-Regulation; Enzyme Inhibitors; Guinea Pigs; Histamine; Male; Neurons; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Recruitment, Neurophysiological; Respiratory System; Serotonin; Vasoactive Intestinal Peptide

Bronchial release appears to be regulated by the nonadrenergic noncholinergic system whose transmitter is very probably VIP. In vivo and in vitro studies were conducted to discover whether peptide modifies basic function and/or bronchial spasm provoked by histamine. The data collected show that VIP failed to cause bronchodilation but protects against histamine induced bronchoconstriction both in vivo and in vitro.

Topics: Adult; Asthma; Bronchi; Bronchial Spasm; Histamine; Humans; In Vitro Techniques; Male; Middle Aged; Muscle Tonus; Spirometry; Vasoactive Intestinal Peptide