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1. It is well established that presynaptic adenosine A1-receptor activation inhibits acetylcholine (ACh) release in the guinea-pig ileum. The present study extends this observation and examines a possible role for endogenous adenosine in modulating cholinergic nerve function. 2. The actions of the adenosine uptake blocker, dipyridamole, the adenosine deaminase inhibitor, erythro-9(2-hydroxy-3-nonyl)adenine (EHNA) and the A1-receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) were examined on electrically evoked neurogenic, cholinergic twitch contractions of the guinea-pig ileum. Some additional studies measuring [3H]-ACh release were also performed. 3. Adenosine and the selective A1-receptor agonist, 2-chloroadenosine (2-CA), inhibited electrically evoked contractions and, in the case of 2-CA, [3H]-ACh release. The actions were antagonized by DPCPX. At low concentrations, dipyridamole and EHNA enhanced the effect of adenosine causing a leftward shift of the concentration-response curve. In contrast, inhibition induced by 2-CA was unaffected by either dipyridamole or EHNA. 4. When applied alone at higher concentrations, EHNA and dipyridamole produced a concentration-dependent suppression of cholinergic neurotransmission. In both cases, the effect could be reversed by DPCPX. At the same concentration, DPCPX alone produced a small but consistent increase in twitch height and [3H]-ACh release. 5. The data confirm the existence of inhibitory presynaptic adenosine A1-receptors modulating cholinergic nerve function in the guinea-pig ileum and suggests that these receptors can be activated by endogenous adenosine released either as adenosine itself or as an ATP metabolite.

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Aim:The present study aimed to investigate toxicity and oral glucose tolerance test (OGTT) of Phyllanthus acidus leaf extract (PAE) on Wistar rat. Methods: PAE was prepared and administered orally to experimental animals used. The extract was tested for toxicity in rats at a dose of 0, 1,000, 1,500 and 2,000 mg/kg body weight p.o once daily for 14 days. The hypoglycemic effects of PAE on normal rats and orally glucose-induced hyperglycemic rats were compared with distilled water and glibenclamide. A single dose (250 mg/kg body weight) of PAE was administered and blood glucose level was obtained by pricking the tail vain using glucometer at time -30, 0, 30, 60, 120 and 240 minutes. Results: All doses of the extract did not exert any sign or symptom of toxicity and the dead rat was not found. The body weight, white blood cell (WBC), mean corpuscular volume (MCV), platelet (PLT), plateletcrit (PCT), mean platelet volume (MPV), platelet distribution width (PDW), blood chemistry, blood urea nitrogen (BUN), creatinine, alkaling phosphatase (ALP) and organ weight of liver were not significantly different between control and treated rats. However, red blood cell (RBC), hematocrit (HCT), lymphocyte (LYM), and hemoglobin (Hb) at a dose 1,500 mg./kg body weight were significantly lower than those in the control group. The blood glucose levels of PAE treated groups were not different with control and Glybenclamide treated. Conclusion: The findings of the present study can be concluded that the PAE are practically non-toxic at a lower dose.

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Two major compounds, stigmasterol (ST) and sitosterol-3-O-β-D-glucopyranoside (SG) were isolated from Pseuderanthemum palatiferum leaf extract which is used traditionally as an antidiabetic. ST and SG at doses of 0.25 and 0.50 mg/kg were fed to diabetic rats for 21 days, and the fasting blood glucose (FBG) level and biochemical data on day 0, 4, 7, 10, 14, 17 and 21 were determined and compared with the anti-diabetic drug, glibenclamine. FBG levels at all doses of ST and SG were significantly decreased (p<0.05) with a concomitant increase in serum insulin. SG at the dose of 0.50 mg/kg showed the highest hypoglycemic effect. ST and SG also improved the following biochemical data and hematology parameters such as total cholesterol, triglycerides, high density lipoprotein (HDL), low density lipoprotein (LDL), blood urea nitrogen, creatinine, red blood cells, platelet and white blood cells.