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Cardiovascular effects of the essential oil of Aniba canelilla bark in normotensive rats.

Abstract
Cardiovascular effects of intravenous (i.v.) treatment with the essential oil of the bark of Aniba canelilla (EOAC) were investigated in normotensive rats. In both pentobarbital-anesthetized and conscious rats, i.v. bolus injections of EOAC (1 to 20 mg/kg) elicited similar and dose-dependent hypotension and bradycardia. Pretreatment of anesthetized rats with bilateral vagotomy significantly reduced the bradycardia without affecting the hypotension. In conscious rats, pretreatment with hexamethonium (30 mg/kg, i.v.) significantly reduced the EOAC-induced bradycardia without affecting the hypotension. The opposite effect was observed after i.v. pretreatment with the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl esther (L-NAME, 20 mg/kg). However, both EOAC-induced hypotension and bradycardia were significantly reduced by pretreatment with methylatropine (1 mg/kg, i.v.). In rat endothelium-containing aorta preparations, EOAC (1-600 microg/mL) induced a concentration-dependent reduction of potassium (60 mM)-induced contraction [IC50 (geometric mean+/-95% confidence interval)=64.5 (45.6-91.2) microg/mL)], an effect that was significantly reduced by the addition of atropine (10 microM) in the perfusion medium [IC50=109.5 (72.5-165.4) microg/mL)]. Furthermore, the vasorelaxant effects of the EOAC were also but significantly reduced [IC50=139.1 (105.2-183.9) microg/mL)] by removal of the vascular endothelium. Furthermore, the CaCl2-induced contractions in calcium-free medium were reduced and even fully abolished by EOAC (100 and 600 microg/mL), respectively. However, EOAC (600 microg/mL) was without significant effect on caffeine-induced contractions in calcium-free medium. These data show that i.v. treatment of rats with EOAC induces dose-dependent hypotension and bradycardia, which occurred independently. The bradycardia appears mainly dependent upon the presence of an operational and functional parasympathetic drive to the heart. However, the hypotension is due to an active vascular relaxation rather than withdrawal of sympathetic tone. This relaxation seems partly mediated by an endothelial L-arginine/nitric oxide pathway through peripheral muscarinic receptor activation (endothelium-dependent relaxation) and predominantly through an inhibition of calcium inward current (endothelium-independent relaxation).
AuthorsSaad Lahlou, Pedro Jorge Caldas Magalhães, Rodrigo José Bezerra de Siqueira, André Fernandes Figueiredo, Leylliane Fátima Leal Interaminense, José Guilherme Soares Maia, Pergentino José da Cunha Sousa
JournalJournal of cardiovascular pharmacology (J Cardiovasc Pharmacol) Vol. 46 Issue 4 Pg. 412-21 (Oct 2005) ISSN: 0160-2446 [Print] United States
PMID16160591 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Central Nervous System Stimulants
  • Oils, Volatile
  • Hexamethonium
  • Caffeine
  • Nitric Oxide Synthase
  • Potassium
  • NG-Nitroarginine Methyl Ester
Topics
  • Animals
  • Aorta, Thoracic (drug effects, physiology)
  • Blood Pressure (drug effects)
  • Caffeine (pharmacology)
  • Cardiovascular System (drug effects)
  • Central Nervous System Stimulants (pharmacology)
  • Consciousness
  • Dose-Response Relationship, Drug
  • Endothelium, Vascular (drug effects, physiology)
  • Heart Rate (drug effects)
  • Hexamethonium (pharmacology)
  • In Vitro Techniques
  • Injections, Intravenous
  • Lauraceae
  • Male
  • Myocardial Contraction (drug effects)
  • NG-Nitroarginine Methyl Ester (pharmacology)
  • Nitric Oxide Synthase (antagonists & inhibitors)
  • Oils, Volatile (administration & dosage, isolation & purification, pharmacology)
  • Plant Bark (chemistry)
  • Potassium (pharmacology)
  • Rats
  • Rats, Wistar
  • Time Factors
  • Vasoconstriction (drug effects)
  • Vasodilation (drug effects)

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