scispace - formally typeset
Search or ask a question

Showing papers on "Arecoline published in 2002"


Journal ArticleDOI
TL;DR: It was found that arecoline acted not only as an inhibitor on gelatinolytic activity of MMP-2, but also a stimulator for TIMP-1 activity, which may contribute to the ECM components accumulation in the areca quid associated OSF.

103 citations


Journal ArticleDOI
TL;DR: A capillary zone electrophoretic method for the rapid analysis of the major alkaloids (arecoline and guavacoline) in areca nut extract is described and is applicable to the analysis of alkaloid in the nut, commercial preparations and in the saliva of areca Nut chewers.
Abstract: A capillary zone electrophoretic (CZE) method for the rapid analysis of the major alkaloids (arecoline and guavacoline) in areca nut extract is described. Areca nuts were pulverized and then extracted with water by sonication in a water bath. After centrifugation, the supernatant was analysed on a fused-silica capillary with 100 mM ammonium acetate-acetic acid (pH 4.6) as the running buffer at a voltage of 20 kV and temperature of 30 degrees C. The method is applicable to the analysis of alkaloids in the nut, commercial preparations (pan masala) and in the saliva of areca nut chewers.

75 citations


Journal ArticleDOI
TL;DR: It is suggested that understanding of the possible pathogenesis for submucous fibrosis through the transformation of normal buccal mucosa as a result of areca quid chewing may be advanced.

44 citations


Journal ArticleDOI
TL;DR: The muscarinic receptor-mediated and non-muscarinic vascular effects of cholinomimetic drugs used in glaucoma were quantified and Physostigmine failed to potentiate the vascular relaxation of exogenous acetylcholine, indicating the absence of acetyl choline esterase in the tissue.
Abstract: The muscarinic receptor-mediated and non-muscarinic vascular effects of cholinomimetic drugs used in glaucoma were quantified. On the isolated rat aorta, the vascular tone induced by phenylephrine is functionally antagonized by cholinomimetic drugs. Based on EC50, the relative order of potency for the endothelium-dependent vascular relaxation was acetylcholine (0.05 microM) 1 > (+/-)-methacholine (0.35 microM) 1/7 > carbachol (0.63 microM) 1/12 > (+/-)-aceclidine (1.26 microM) 1/25. The maximal effects of the four agonists varied between 82-87%. The muscarinic vascular relaxation of 0.03 microM to 100 microM pilocarpine was less than 15%. At high concentrations, pilocarpine had 1/20.000 the vascular activity of acetylcholine. Physostigmine failed to potentiate the vascular relaxation of exogenous acetylcholine, indicating the absence of acetylcholine esterase in the tissue. Arecoline, with an EC50 of 7.76 microM, was partly sensitive to the removal of the endothelium. Atropine treatment did not block the vascular effect of high concentrations of pilocarpine. Atropine, as expected, blocked the vascular effects of carbachol with K(B) = 3.2 nM. Pilocarpine produces vascular relaxation by its competition with spasmogens like phenylephrine, oxymetazoline, vasopressin or latanoprost. Arecoline also shares these properties with pilocarpine in the blood vessel. The molecular mechanism of the vascular effects as well as ocular clinical implications of cholinomimetic drugs is discussed.

12 citations


Journal ArticleDOI
TL;DR: Chronic betel quid use does not seem to affect the assessment of 24h energy expenditure provided that subjects are denied access to betel nut usage before and during calibration.
Abstract: Background : The betel-nut quid, a piece of areca nut chewed alone or mixed with tobacco and slaked lime wrapped in betel vine leaf, is widely used in Asian populations as a stimulant (due to the cholinergic agent, arecoline) or as a relaxant (due to arecaidine and guvacine). Objectives : This study, which formed part of a larger project assessing the effect of energy expenditure on the duration of post-partum amenorrhoea, provided the opportunity to assess the role of chronic areca nut usage on heart rate and oxygen consumption during resting periods and during graded stepping tests. Subjects and methods : The mothers ( n = 47), all of whom were lactating, were aged between 19 and 39, of low nutritional status and anaemic and they all chewed betel quid daily. Results : Moderate users of betel quid (defined as more than 3 times a day) were found, on average, to have a significantly lower heart rate at rest and during exercise than low betel quid users (less than 3 times a day) but there was no modificatio...

7 citations


Journal Article
TL;DR: The antithrombotic effects of arecoline are associated with activating the endothelial target for acetylcholine closely, but are not associated with muscarinic receptors, and not relevant to hemostatic systems or functions of platelet aggregation directly.
Abstract: AIM To examine antithrombotic effects of arecoline on the arterial thrombosis induced by carrageenin in mice through modulating the functions of endothelium and determine its mechanisms from hemostatic system, the platelet aggregative functions and the bioactive factors released by vascular endothelial cells. METHODS Kappa carrageenin was given ip in mice and mice were fed at the temperature of 20 to 21 degrees and at the humidity of 30 percent to 50 percent. RESULTS On the foregoing models of thrombosis, arecoline could antagonize the formation of thrombosis through activating the endothelial target for acetylcholine in a dose dependent manner and its antithrombotic potency was 250 to 500 times greater than aspirin; while under the same conditions, pilocarpine could not antagonize the formation of thrombosis. The levels of TT, PT, KPTT and MAR had no prominent changes compaired with control groups. The levels of t-PA became higher greatly than normal and the levels of PAI 1 became lower greatly than normal 2 hours after intravenous injection of arecoline in rats. Arecoline could decrease the higher plasma levels of thromboxane A2 and increase the lower plasma levels of prostacyclin in a dose dependent manner in the mice tail thrombosis induced by carrageenin. CONCLUSION The antithrombotic effects of arecoline are associated with activating the endothelial target for acetylcholine closely, but are not associated with muscarinic receptors,and not relevant to hemostatic systems or functions of platelet aggregation directly.

5 citations


Journal ArticleDOI
TL;DR: The data suggest that the underlying mechanism by which phosphoinositide turnover is inhibited is arecoline‐induced receptor sequestration.
Abstract: To understand the effects of arecoline administration on the muscarinic cholinergic signaling pathway, rats were injected with arecoline, 10 mg/kg i.p., and the carbachol-stimulated phosphoinositide breakdown in rat brain cortical slices was examined. In vivo administration of arecoline resulted in inhibition of carbachol-stimulated phosphoinositide turnover in rat brain cortical slices. Arecoline was a partial agonist with peak effects of 30% of the maximum as obtained with carbachol. Coaddition of arecoline inhibited the carbachol-stimulated phosphoinositide breakdown. Pretreatment of rat brain cortical slices with arecoline in vitro resulted in a dose-dependent inhibition of carbachol-stimulated [3H]inositol monophosphate accumulation. The inhibition occurred rapidly, with half-maximal inhibition occurring at 15 min and maximal inhibition achieved within 60 min. The inhibition of phosphoinositide breakdown was recovered 1 h after arecoline was removed. When synaptoneurosomes were used for the ligand binding studies, arecoline pretreatment was found to have decreased the maximal ligand binding (Bmax) without inducing any marked change in binding affinity (K(D)). The influence could be recovered by incubating the synaptoneurosomes in the absence of arecoline for 2 h. Taken together, these data suggest that the underlying mechanism by which phosphoinositide turnover is inhibited is arecoline-induced receptor sequestration.

3 citations