Role of GABA[B] receptor and L-Arg in GABA induced vasorelaxation in non-diabetic and streptozotocin- induced diabetic rat vessels

Hypertension is considered an independent risk factor for cardiovascular mortality in diabetic patients. The present study was designed to determine the role of gamma amino butyric acid B [GABA[B]] receptor and L-arginine [L-Arg] in GABA-induced vasorelaxation in normal and streptozotocin-induced diabetic rat vessels. Diabetes was induced by a single i.p. injection of streptozotocin [STZ, 60 mg/kg]. Eight weeks later, superior mesenteric arteries of all groups were isolated and perfused according to the McGregor method. Baseline perfusion pressure of STZ diabetic rats was significantly higher than non-diabetic rats in both intact and denuded endothelium. In the presence of faclofen, a selective GABA[B] receptor blocker, GABA-induced relaxation in intact and denuded endothelium mesenteric beds of STZ diabetic rats was suppressed, but this response in nondiabetic rats was not suppressed. Our results showed that in the presence of L-Arg, a nitric oxide precursor, GABA induced vasorelaxation in both diabetic and non-diabetic vessels. From the results of this study, it may be concluded that the vasorelaxatory effect of GABA in diabetic vessel is mediated by the GABA[B] receptor and nitric oxide, but it seems that in non-diabetic vessel GABA[B] receptor does not play any role in GABA-induced vasorelaxation, but nitric oxide induced GABA relaxation in non-diabetic vessel

commemorating one thousandth anniversary of the avicenna's canon of medicine: gastric headache, a forgotten clinical entity from the medieval Persia

Although the connection between head and stomach and hence the condition known as [gastric headache] was well known to the ancients, it has received little attention since the early 20[th] century. Herein, we review the teachings of the medieval Persian physicians about the gastric headache along with the related signs, symptoms, types and causes. The medieval Persian scholars adopted the main ideas of the gastric headache from predecessors in the ancient Greece and Rome, added substantial sub-categories and details to the earlier descriptions and therapeutic options. The medieval Persian physicians' contributions to the concept of gastric headache influenced beyond doubt the later accounts of this condition

Relaxatory effect of gamma-aminobutyric acid [GABA] is mediated by same pathway in diabetic and normal rat mesenteric bed vessel

Diabetes related dysfunction of resistance vessels is associated with vascular occlusive diseases. Vasorelaxant agents may have a role in control of diabetic cardiovascular complications. Gamma aminobutyric acid [GABA] has demonstrated to cause vasorelaxation. The present study was designed to determine i] the vasorelaxatory effect of GABA on diabetic vessels and ii] the role of endothelium in GABA-induced vasorelaxation. After Diabetes induction,. Mesenteric arteries of animals were perfused. Vascular beds were constricted with phenylephrine. GABA [1 to 50 micro M] was added into the medium and perfusion pressure was then recorded. In all groups of animals, relaxant response to GABA in mesenteric bed appeared. Although diabetes induction did not change mesenteric bed response to GABA, denuded vessels showed a reduced response to GABA both in control and diabetic animals. GABA can induce endothelium dependent vasorelaxation in mesenteric vessels in normal and diabetic rats

Lead exposure changes gastric acid secretion in rat: role of nitric oxide [No]

Sub chronic exposure to lead in rats slows gastric emptying, but little is known about the effects of lead on gastric secretion. This study was designed to investigate the effects of lead on gastric acid secretion and its possible mechanisms in rats. Lead acetate was dissolved in drinking water in a concentration of 1%. Sodium acetate-containing water with a molar concentration similar to lead was also prepared. We had nine groups of animals [n=8]; four of them were exposed to lead for 1, 2, 3, and 4 weeks [Pbl, Pb2, Pb3 and Pb4 groups, respectively]. Sodium acetate solution was given to another four groups for 1, 2, 3, and 4 weeks [Nal, Na2, Na3 and Na4 groups, respectively]. Gastric secretion was collected by washout technique and its acid output was measured in the basal [Basal Acid Output, BAO], vogotomy [Vagotomized Acid Output, VAO], and vagally stimulated [Vagally Stimulated Acid Output, VSAO] states using titrator instrument. Nitric oxide [NO] metabolite of gastric tissue was determined by Griess micro assay method to evaluate the possible mechanism of lead effect on gastric secretion. VSAO was significantly less in Pbl and Pb2 groups than Nal and Na2 ones respectively [1.75 +/- 0.17, 2.10 +/- 0.30 vs. 5.79 +/- 0.20, 6.18 +/- 0.27 micromol/15min] [P=0.001, P=0.001] BAO was significantly more in Pb3 and Pb4 groups than Na3 and Na4 ones respectively [2.77 +/- 0.37, 2.80 +/- 0.31 vs. 1.73 +/- 0.16, 1.79 +/- 0.34 micromol/15min] [P=0.01, P=0.02], but it was the same after vagotomy. VSAO was more in Pb3 and Pb4 groups than their Na counterparts [P=0.001, P=0.0001] NO metabolite of gastric tissue was more in all Pb groups in comparison to their Na counterparts [P=0.0001]. In this study, it seems that lead exposure, via NO mechanism, has different effects on acid secretion. Nitric oxide in small and large amounts decrease and increase gastric acid secretion, respectively

Temperature changes during and after eccentric contractions and its effect on force and desmin loss in rat

The typical features of eccentric exercise-induced muscle damage is prolonged loss of muscle strength and the most rapid structural change in the fibers is loss of immunostaining for the intermediate filament protein, desmin. In this study isolated perfused rat muscle was used to examine the direct effect of temperature changes on the eccentric contraction-induced force and desmin loss. The left medial gastrocnemius muscle was separated and the entire lower limb was transferred into a prewarmed [35 Degree C] organ bath. Temperature was adjusted to 31 or 39 Degree C during and after eccentric contractions. Maximal isometric force and desmin loss were measured after 15 isometric or eccentric contractions. According to our data, organ bath temperature changes during or after eccentric contractions had no significant effect on force loss. However, a strong correlation between desmin loss and temperature changes during [r = 0.886, P< 0.05] and a weak correlation between desmin loss and temperature changes after [r= 0.699, P<0.05] eccentric contractions was observed. Our results suggest that cooling during eccentric contractions may decrease desmin loss but temperature changes after eccentric contractions have no effect on desmin loss

Lead exposure changes gastric motility in rats: role of nitric oxide [no]

Abdominal colic, constipation and delay in gastric emptying are symptoms of lead poisoning, but there is scant information about the effect of lead on gastric motility. In the present study, we investigated the effect of lead acetate on gastric motility in rats. Animals were divided into nine groups [n=8]; four groups were exposed to lead acetate solution [1%] for 1, 2, 3, and 4 weeks [Pb1, Pb2, Pb3, and Pb4 groups, respectively]. Sodium acetate solution was given to another four groups for 1, 2, 3, and 4 weeks [Na1, Na2, Na3, and Na4 groups, respectively] and the control group had free access to tap water. Gastric motility was measured in the basal and acetylcholine [Ach]-stimulated states using a physiograph instrument. Nitric oxide metabolite of gastric tissue was determined by Griess micro-assay. There were no significant differences between basal and Ach-stimulated gastric motility in Pb1, Pb2, Na1, and Na2 groups. However, it was significantly greater in Pb3 and Pb4 groups when compared with Na3 and Na4 groups in both basal and Ach-stimulated states [P<0.05]. In addition, nitric oxide metabolite of gastric tissue was more in all Pb groups in comparison with their Na counterparts [P<0.05]. We found that lead exposure could affect gastric motility via the nitric oxide pathway

effect of [teucrium polium l.] extracts on insulin release from in situ isolated perfused rat pancreas in a newly modified isolation method: the role of ca[2+] and k[+] channels

[Teucrium polium L] [TP] has been long recommended in Iranian folk medicine for its anti-diabetic activities. We attempt here to evaluate the effect of TP extract on insulin secretion in rat pancreas. Rat pancreas was isolated in situ and perfused with Krebs solution containing low glucose [LG, 2.8 mM] or high glucose [HG, 16.7 mM] as perfusate. The aqueous extract [Aq. E] and methanolic extract [Met. E] of TP aerial parts and two partition fractions of Met. E were added to perfusate to evaluate insulin release. Diazoxide [DZX] and verapamil [VPM] were also used for assessing the probable mechanism of the effects. In each experimental group, the peak and baseline of insulin levels in effluent samples were compared. The GC/MS analysis was carried out to detect active ingredients in the extracts. Adding Met. E to the LG caused a significant increase [P<0.05] in insulin release from the basal level of 0.17 +/- 0.05 micro g/1 to a peak value of 3.94 +/- 1.29 micro g/1, when Met. E was introduced to the HG, there was a further protracted stimulation of insulin release from 2.15 +/- 1.35 micro g/1 to 6.16 +/- 0.52 micro g/1. Both DZX and VPM when added separately to the LG, led to inhibition of Met. E induced insulin secretion. The Aq. E and fractions had no significant effect on insulin secretion. Only in the Met. E, the component 5-hydroxy-4.7-dimethoxyflavone [apigenin-4,7-dimethylether] was detected. It can be concluded that the insulinotropic properties of TP extracts can be attributed to the presence of apigenin existing only in Met. E, but not in Aq. E and fractions. Moreover, certain types of K[+] and Ca[2+] channels take part in this effect

Prenatal alcohol exposure and dysfunction of hippocampal formation in cognition

Background: Fetal alcohol syndrome is associated with numerous problems in the development and function of the brain. Learning and memory deficits are among well known effects of prenatal exposure to alcohol

Objective: This study aimed to examine the spatial working memory of 60-day old rats who were exposed to alcohol during their fetal life and to find the relation between the possible alcohol-impaired spatial memory and gestational period of exposure to alcohol

Materials and Methods: Pregnant rats in different stages of gestation period were administered with ethanol. Using a radial arm maze, the offspring were subjected to spatial working memory training at 60 days of postnatal age

Results: The rats exposed to ethanol during the first 10 days of fetal life indicated lower performances compared to the controls. Those receiving alcohol during the second half of pregnancy period had no problem in maze navigation. Behavior of the animals exposed to alcohol during the first and the second quarter of the gestation period demonstrated that only the latter were weak in solving maze tasks. The groups related to the third and the forth quarter of gestation period had a similar behavior with the control group. Comparison of the animals' performances in all groups revealed that only the second quarter group was the most disadvantaged

Conclusion: Our data indicates that the second quarter of the gestation period is more sensitive to harmful effects of alcohol on the areas of brain involved in learning and memory. Since the hippocampus is central in cognitive functions and this part of brain is highly vulnerable to alcohol effects it can be concluded that the hippocampus is mostly affected in the second quarter of prenatal life