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Cardiovascular effects of 1‐nitro‐2‐phenylethane, the main constituent of the essential oil of Aniba canelilla , in spontaneously hypertensive rats
Author(s) -
Interaminense Leylliane de Fátima Leal,
de Siqueira Rodrigo José Bezerra,
Xavier Fabiano Elias,
Duarte Gloria Pinto,
Magalhães Pedro Jorge Caldas,
da Silva Joyce Kelly,
Maia José Guilherme Soares,
Sousa Pergentino José da Cunha,
LealCardoso José Henrique,
Lahlou Saad
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.1472-8206.2010.00891.x
Subject(s) - capsazepine , guanethidine , phenylephrine , vagus nerve , vagotomy , stimulation , reflex , capsaicin , chemistry , anesthesia , contraction (grammar) , vasodilation , medicine , endocrinology , pharmacology , trpv1 , blood pressure , receptor , transient receptor potential channel
This study investigated the cardiovascular responses to the essential oil of Aniba canelilla (EOAC) and its main constituent 1‐nitro‐2‐phenylethane (NP) in spontaneously hypertensive rats (SHRs). In anesthetized SHRs, intravenous (i.v.) bolus injections of EOAC (1–20 mg/kg) or NP (1–10 mg/kg) elicited dose‐dependent hypotensive and bradycardiac effects, which were characterized in two periods (phases 1 and 2). The first rapid component (phase 1) evoked by EOAC and NP both at 10 mg/kg was absent after left ventricle injection, fully abolished by bilateral vagotomy and perineural treatment of both cervical vagus nerves with capsaicin (250 μg/mL) while remained unaltered by i.v. pretreatment with capsazepine (1 mg/kg) or ondansetron (30 μg/kg). In conscious SHRs, NP (5 and 10 mg/kg, i.v.) evoked rapid hypotensive and bradycardiac effects (phase 1) that were fully abolished by methylatropine (1 mg/kg, i.v.) pretreatment. In rat endothelium‐containing mesenteric preparations, increasing concentrations (0.1–1000 μg/mL) of EOAC and NP relaxed the phenylephrine‐induced contraction in a concentration‐dependent manner. It is concluded that NP induces a vago‐vagal bradycardiac and depressor reflex (phase 1) that apparently results from the stimulation of vagal pulmonary rather than cardiac C‐fiber afferents. This effect does not appear to involve activation of either vanilloid TPRV 1 or 5‐HT 3 receptors located on vagal sensory nerves. The phase 2 hypotensive response to i.v. NP seems to result, at least in part, from its direct vasodilatory effect on the peripheral smooth muscle. All in vivo and in vitro effects of EOAC are mostly attributed to the actions of its main constituent NP.