Pharmacological evidence of calcium‐channel blockade by essential oil of Ocimum gratissimum and its main constituent, eugenol, in isolated aortic rings from DOCA‐salt hypertensive rats

Abstract

Intravenous (i.v.) treatment of conscious DOCA-salt hypertensive rats with the essential oil of Ocimum gratissimum L. (Labiatae) (EOOG) induced a hypotensive effect that seems related to an active vascular relaxation rather than withdrawal of sympathetic tone. To corroborate this hypothesis, the present study examined the vascular effects of EOOG and its main constituent, eugenol (EUG) and the putative mechanisms underlying these effects. Additionally, the role of the vascular beta(2)-adrenergic mechanism in the mediation of EOOG-induced hypotension has also been investigated. In conscious DOCA-salt hypertensive rats, the EOOG-induced hypotension was reversible and remained unchanged by i.v. pretreatment with propranolol (2 mg/kg). In isolated aorta preparations with intact endothelium from DOCA-salt hypertensive rats, EOOG (1-1000 microg/mL) and EUG (0.006-6 mM) relaxed the phenylephrine-induced contraction similarly with IC(50) [geometric mean (95% confidence interval)] values of 226.9 (147.8-348.3) microg/mL and 1.2 (0.6-2.1) mm, respectively. Vasorelaxant effects of EOOG were significantly altered by removal of the vascular endothelium [IC(50) = 417.2 (349.5-497.8) microg/mL]. In a calcium-free medium, the CaCl(2)-induced contractions were significantly reduced and even abolished by EOOG at 300 and 1000 microg/mL, respectively, whereas EOOG (1000 microg/mL) did not have any significant effect on caffeine-induced contractions. Similar results were obtained with EUG (1.8 and 6 mM) on both CaCl(2)- and caffeine-induced contractions, respectively. The data suggest that hypotensive responses to EOOG in DOCA-salt hypertensive rats are due to an active vascular relaxation, which is partly dependent upon the integrity of the vascular endothelium and seems predominantly mediated through an inhibition of plasmalemmal Ca(2+) influx rather than Ca(2+)-induced Ca(2+) release from the sarcoplasmic reticulum.