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1.
Article | IMSEAR | ID: sea-188023

ABSTRACT

Aims: One of the most important causes of mortality is vascular complications resulting from diabetes mellitus. Herbal medicines are commonly used for the treatment of cardiovascular conditions in diabetes. Artemisia annua (A. annua) as a medicinal plant has vasculature protective effects in diabetic rats. In the present study, the role of prostaglandins in the vasodilator effect of A. annua aqueous extract in diabetic rats has been studied. Study Design: This animal study was conducted on diabetic rats. Aqueous extract of Artemisia annua was used for diabetic rats. Then, isolated thoracic aortic rings were exposed to indomethacin and after exposure, the contractile responses were measured. Methodology: The studied animals were male Wistar rats (n=36) which were randomly divided into intact, untreated-diabetic, and A. annua aqueous extract treated-diabetic groups. For the induction of diabetes, streptozotocin was intraperitoneally (i.p.) administered (60 mg/kg). A. annua extract-treated group received i.p. 100 mg/kg of extract for one month. After one month, the dose contractile response of isolated aortic rings to phenylephrine (doses of 10-9-10-4 mol/L) in the absence and presence of indomethacin as a prostaglandins inhibitor was determined using isolated tissue setup. Results: Comparison of contractile responses before and after adding indomethacin in treated extract diabetic rats, showed that contractile responses of aorta ring with and without endothelium after adding indomethacin significantly increased at all concentrations of phenylephrine (P<0.05–P<0.0001) while indomethacin in diabetic rats did not effect on contractile response. Conclusions: Since the vasodilator effect of the aqueous extract of A. annua with a concentration of 100 mg/kg of body weight was pronounced even after endothelium removal, it can be claimed that the vasodilator effects of the extract are related to inhibition of prostaglandin generation both indirectly and directly.

2.
Chinese Pharmacological Bulletin ; (12): 1131-1135, 2017.
Article in Chinese | WPRIM | ID: wpr-613660

ABSTRACT

Aim To investigate the effects of midazolam on porcine isolated coronary artery rings pre-contracted by potassium chloride(KCl)and the possible mechanism.Methods The vessel tension recorder system was used.Isotonic tension of porcine isolated coronary artery rings precontracted by KCl(30 mmol·L-1)was recorded.The vasorelaxing action of midazolam and effects of various drugs were observed in the rings.Results Midazolam(3×10-6~1×10-4 mol·L-1)respectively concentration-dependently reduced the contraction induced by KCl,and there was significant difference between the rings with intact and denude endothelium(P<0.05).On KCl-induced precontraction,midazolam′s relaxation was depressed by L-NAME and the blend of L-NAME and L-Arg(P<0.05),but was not affected by Indo,L-Arg and 1400W.The contraction was not prevented by pretreatment with the inhibitor of Na+/Ca2+ exchanger(KB-R7943).The inhibitor of KATP(Gli)restrained the diastolic function of midazolam(P<0.05),while the inhibitor of BKCa(TEA),Kir(BaCl2),KV(4-AP)had no obvious effect.Conclusions Midazolam produces remarkable vasodilatation on KCl pre-contracted porcine isolated coronary artery rings.Its relaxtion effect is via concentration-dependent and endothelium-dependent mechanisms and relevant to the production of NO.Na+/Ca2+ exchanger is not involved midazolam′s vasodilatation on KCl pre-contracted porcine coronary artery rings.The relaxant mechanism of midazolam may be concerned with KATP.The Kir,BKCa and KV may be not involved.

3.
Chinese Pharmacological Bulletin ; (12): 554-558, 2016.
Article in Chinese | WPRIM | ID: wpr-484538

ABSTRACT

Aim To investigate the vasodilatory effect of Ferulic acid on in vitro rat coronary artery and its possible mechanism. Methods By using the mi-crovessel tension recorder system, the vasodilatory effect of FA on resting and contractin-vitro rat coronary artery was determined;the influence of endothelial in-tegrity to FA-induced vasorelaxation was observed; the relationship of FA on [ Ca2+] ex-influx-induced and [ Ca2+] in-efflux-induced contractions was discussed;the mechanism of vasodilatory effect of FA was ex-plored by applying the inhibitors of KCa(TEA),KATP channel ( Gli ) , KIR channel ( BaCl2 ) , KV ( 4-AP ) , NOS( L-NAME) and COX( Indo) . Results FA had no effect on the resting tension of in vitro rat coronary artery. FA dilated the in-vitro rat coronary artery pre-treated with KCl ( 60 mmol · L-1 ) , U46619 ( 1 μmol · L-1 ) and PE ( 10μmol · L-1 ) in a concentration-dependent fashion ( P 0. 05 ) . Conclusion The diastolic func-tion could be related to the activation of KV channel on vascular smooth muscle cells, the free Ca2+ from Sar-coplasmic reticulum cells and blockade extracellular Calcium channel do not depend on KCa, KATP, KIR channel, nor the endothelial function.

4.
China Pharmacist ; (12): 884-887, 2015.
Article in Chinese | WPRIM | ID: wpr-669754

ABSTRACT

Objective:To investigate the vasorelaxant effect of active fraction from compound Prunella vulgaris L. ( AFCP) on the i-solated thoracic aorta of rats and underlying mechanism. Methods:The study was performed with the tension experiment of the isolate rat thoracic aorta. The changes of vascular ring tension were measured by biological signal acquisition and analysis system, and the vasodila-tor effect of AFCP was observed. Results:AFCP(100-500μg·ml-1)could induce significant relaxation in aorta rings pre-contracted by phenylephrine (PE,1 μmol·L-1), and the relaxation effect was significant(75% ±8%) in endothelium-intact aortic and endothelium-denuded aortic. The vasodilatation effect of AFCP was not significantly affected by nitric oxide synthase ( NOS) inhibitor NG-nitro-L-argi-nine( L-NNA) , guanylate cyclase inhibitor MB,potassium channel blocker TEA and glibenclamide. In Ca2+-free bath solutions, AFCP (300 μg·ml-1 ) could shift downward dose-response curve of CaCl2 and significantly reduce the maximum contraction amplitude of PE. Conclusion:AFCP can relax rat aorta rings in a dose-dependent manner, which is endothelium-independent. The mechanism may be re-lated to the inhibition of intracellular calcium release and extracellular calcium flow, and has nothing to do with NO pathway, prostacyclin generation and calcium-activated potassium channels.

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