Influence β-Eudesm on blood pressure and aortic strips contractility of the rat

Abstract

일후박(日厚朴, Magnolia obovata Thunberg)의 수피에는 여러 성분이 함유되어 있으며, 정유성분으로 β-eudesmol, α- 및 β-pinenes, 그리고 bornyl acetate등이 있으며, 또한 디페닐 화합물로는 magnolol 과 honokiol, 그리고 알칼로이드 성분으로 magnocurarine 과 magnoflorine이 알려져 있다. 최근 임등(2003)은 마취 흰쥐에서 bornyl acetate 가 아드레날린 α_(1)-수용체를 차단함으로써 혈압하강을 나타내며 α_(1)-아드레날린 수용체의 차단작용에 의한 혈관이완작용을 나타낸다고 하였다. Tachikawa 등 (2000)은 일후박 추출물이 소의 부신 크롬친화세포에서 아세칠콜린에 의한 카테콜아민 분비작용을 억제한다고 하였다. 따라서, 본 연구는 β-eudesmol 가 정상혈압 쥐에서 혈압반응과 적출혈관 평활근의 수축반응에 대한 β-eudesmol 의 효과를 검색하고 작용기전을 규명하고자 수행하였다. Phenylephrine (α_(1)-아드레날린 수용체 효능약)과 고농도 칼륨(막탈분극약)은 적출 대동맥 편에서 각각 현저한 수축반응을 일으켰다. 이 같은 고농도칼륨 (5.6X10^(-2) M)에 의한 수축반응은 β-eudesmol (10~40 μg/ml) 존재 하에서 용량-의존적으로 억제되었다. 또한 phenylephrine (10^(-5)M)에 의한 수축반응도 β-eudesmol (10~40 μg/ml) 존재 하에서는 용량 의존적인 억제작용을 나타내었다. 더욱이, β-eudesmol (3 mg/kg/30min)을 정상혈압의 urethane 마취흰쥐에서 정맥 내로 30분간 주입시 norepinephrine에 의한 승압반응을 현저히 억제하였다. 이상과 같은 연구결과를 종합하여보면, 마취흰쥐에서 정맥 내로 투여한 β-eudesmol은 적어도 아드레날린 α_(1)-수용체를 차단함으로써 혈압하강을 나타내는 것으로 생각되며, 또한 β-eudesmol은 기전 미상의 직접작용 외에 α_(1)-아드레날린 수용체의 차단작용에 의한 혈관이완작용을 나타내는 것으로 사료된다. 또한 β-eudesmol과 bornyl acetate는 작용양식에 있어서 차이가 없는 것 같다.|It has been found that various other ingredients have been isolated and identified from the bark of Magnolia obovata Thunberg (日厚朴), a medicinal plant. They are (β-eudesmol, α- and β-pinenes, and bornyl acetate, as essential oils; magnolol and honokiol, as diphenyl compounds; and magnocurarine and magnoflorine, as alkaloids. Recently, Lim and his co-workers (2003) have reported that intravenous bornyl acetate, one of active components of magnolia bark, causes the depressor action in the anesthetized rat at least partly through the blockade of adrenergic α_(1)-receptors, and it also causes vascular relaxation in the isolated aortic strips of the rat via the blockade of adrenergic α_(1)-receptors. The crude extract of magnolia bark is found to inhibit the secretion of catecholamines from bovine adrenal chromaffin cells stimulated by acetylcholine in a concentration-dependent manner (Tachikawa et al., 2000). Therefore, the present study was conducted to investigate the effects of β-eudesmol on arterial blood pressure and vascular contractile responses in the normotensve rats and to establish the mechanism of action. Phenylephrine (an adrenergiα_(1)-receptor agonist) and high potassium (a membrane-depolarizing agent) caused greatly contractile responses in the isolated aortic strips, respectively. These phenylephrine (10^(-5) M)-induced contractile responses were depressed in the presence of high concentrations of β-eudesmol (10 ~ 40 μg/ml), but not affected in low concentration of β-eudesmol (2.5 ~ 5 μg/ml). Also, high potassium (5.6 x 10^(-2) M)-induced contractile responses were greatly inhibited in the presence of β-eudesmol (10 ~ 40 μg/ml) in a dose-dependent fashion. β-Eudesmol (1 ~ 10 mg/kg) given into a femoral vein of the normotensive rat produced a dose-dependent depressor response, which is transient (data not shown). Interestingly, the infusion of a moderate dose of β-eudesmol (3 mg/kg/30 min) made a significant reduction in pressor responses induced by intravenous norepinephrine. Collectively, these results obtained from the present study demonstrate that intravenous β-eudesmol causes a dose-dependent depressor action in the anesthetized normotensive rat at least partly through the blockade of adrenergic α_(1)-receptors. β-Eudesmol also causes vascular relaxation in the isolated aortic strips of the rat via the blockade of adrenergic α_(1)-receptors, in addition to the unknown mechanism of the direct vasorelaxation. It seems that there is no difference in mode of action between bornyl acetate and β-eudesmol.