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Antispasmodic effects of eugenol on rat airway smooth muscle
Author(s) -
Lima Felipe Crescêncio,
PeixotoNeves Dieniffer,
Gomes Maria Diana Moreira,
CoelhodeSouza Andrelioronha,
Lima Crystianne Calado,
Araújo Zin Walter,
Magalhães Pedro Jorge Caldas,
Saad Lahlou,
LealCardoso José Henrique
Publication year - 2011
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2010.00892.x
Subject(s) - eugenol , nifedipine , chemistry , stimulation , endocrinology , contraction (grammar) , medicine , muscle contraction , antispasmodic , agonist , pharmacology , receptor , calcium , biochemistry , organic chemistry
This study was undertaken to assess the effects of eugenol (EUG) on tracheal muscle (TM) and the putative mechanisms underlying these effects. Cumulatively increasing concentrations (1–1000 μ m ) of EUG did not affect the resting tonus of TM. However, EUG (1–2000 μ m ) reduced the contractions induced by electrical field stimulation (IC 50 = 842.3 ± 52.7 μ m ), an effect that was unaltered by either 10 μ m montelukast (IC 50 = 816.1 ± 70.1 μ m ) or 2 μ m indomethacin (IC 50 = 693.1 ± 170.8 μ m ). EUG also completely relaxed the sustained contractile responses to 80 mM K + (IC 50 = 597.3 ± 60.6 μ m ) and 1 μ m carbamoylcholine (IC 50 = 571.3 ± 148.8 μ m ), an effect that was unaltered by indomethacin (2 μ m ). Under Ca 2+ ‐free conditions, EUG reduced the ACh‐induced contractions (IC 50 = 703.4 ± 256.1 μ m ), the CaCl 2 ‐induced contractions in preparations pretreated with 60 μ m ACh in the presence of nifedipine, and the Ba 2+ ‐induced contractions in preparations depolarized with K + . In tracheal preparations maintained in Ca 2+ ‐containing solution, EUG (300–2000 μ m ) relaxed the contractile response to phorbol dibutyrate (1 μ m ), an activator of protein kinase C. It is concluded that in TM, EUG induces a myogenic antispasmodic effect (not modulated by arachidonic acid derivatives) either through various mechanisms almost with the same pharmacological potency or via an action on a step common to all of them. These mechanisms seem to include blockade of voltage‐ and receptor‐operated Ca 2+ channels, IP 3 ‐induced Ca 2+ release from sarcoplasmic reticulum and reduction of the sensitivity of contractile proteins to Ca 2+ .