Acute physical and psychological stress effects on visceral hypersensitivity in male rat: role of central nucleus of the amygdala / Efeitos agudos do estresse físico e psicológico na hipersensibilidade visceral em rato macho: papel do núcleo central da amídala

ABSTRACT Objective: The aim of this study was to investigate the effects of acute physical and psychological stress and temporary central nucleus of the amygdala (CeA) block on stress-induced visceral hypersensitivity. Methods: Forty two male Wistar rats were used in this study. Animals were divided into 7 groups (n = 6); 1 - Control, 2 - physical stress, 3 - psychological stress, 4 - sham, 5 - lidocaine, 6 - lidocaine + physical stress and 7 - lidocaine + psychological stress. Stress induction was done using a communication box. Results: Abdominal withdrawal reflex (AWR) score was monitored one hour after stress exposure. AWR score significantly heightened at 20, 40 and 60 mmHg in the psychological stress group compared with control (p < 0.05), while, it was almost unchanged in other groups. This score was strikingly decreased at 20, 40 and 60 mmHg in lidocaine + psychological stress group compared with psychological stress with no tangible response on physical stress. Total stool weight was significantly increased in psychological stress group compared with control (0.72 ± 0.15, 0.1 ± 0.06 g) (p < 0.05), but it did not change in physical stress compared to control group (0.16 ± 0.12, 0.1 ± 0.06 g) (p < 0.05). Concomitant use of lidocaine with stress followed the same results in psychological groups (0.18 ± 0.2, 0.72 ± 0.15 g) (p < 0.05), while it did not have any effect on physical stress group (0.25 ± 0.1, 0.16 ± 0.12 g) (p < 0.05). Conclusions: Psychological stress could strongly affect visceral hypersensitivity. This effect is statistically comparable with physical stress. Temporary CeA block could also reduce visceral hypersensitivity post-acute psychological stress.

RESUMEN Objetivo: O objetivo desse estudo foi investigar os efeitos do estresse físico e psicológico agudo e bloqueio temporário do núcleo central da amídala (CeA) na hipersensibilidade visceral induzida por estresse. Métodos: Quarenta e dois ratos Wistar machos foram empregados nesse estudo. Os animais foram divididos em 7 grupos (n = 6): 1 - Controle, 2 - estresse físico, 3 - estresse psicológico, 4 - simulacro, 5 - lidocaína, 6 - lidocaína + estresse físico e 7 - lidocaína + estresse psicológico. A indução do estresse foi feita com o uso de uma caixa de comunicação. Resultados: O escore do reflexo de retirada abdominal (RRA) foi monitorado uma hora depois da exposição ao estresse. O escore RRA aumentou significativamente a 20, 40 e 60 mmHg no grupo de estresse psicológico versus controle (p < 0,05), enquanto que praticamente permaneceu inalterado nos demais grupos. Esse escore diminuiu drasticamente a 20, 40 e 60 mmHg no grupo de lidocaína + estresse psicológico versus estresse psicológico, sem resposta tangível no estresse físico. O peso total das fezes aumentou significativamente no grupo de estresse psicológico versus controle (0,72 ± 0,15, 0,1 ± 0,06 g) (p < 0,05), mas não houve mudança no grupo de estresse físico versus controle (0,16 ± 0,12, 0,1 ± 0,06 g) (p < 0,05). O uso simultâneo da lidocaína com o estresse acompanhou os mesmos resultados nos grupos psicológicos (0,18 ± 0,2, 0,72 ± 0,15 g) (p < 0,05), enquanto que não foi observado qualquer efeito no grupo de estresse físico (0,25 ± 0,1, 0,16 ± 0,12 g) (p < 0,05). Conclusões: O estresse psicológico pode afetar fortemente a hipersensibilidade visceral. Esse efeito é estatisticamente comparável com o estresse físico. Um bloqueio temporário do CeA também pode reduzir a hipersensibilidade visceral pós-estresse psicológico agudo.

Smart bomb AS1411 aptamer-functionalized/PAMAM dendrimer nanocarriers for targeted drug delivery in the treatment of gastric cancer.

Chemotherapy, a conventional method assessed in recent oncology studies, poses numerous problems in the clinical environment. To overcome the problems inherent in chemotherapy, an intelligent drug delivery system has come to the forefront of cancer therapeutics. In this study, we designed a dendrimer-based pharmaceutical system together with a single-stranded AS1411 aptamer (APTAS1411 ) as a therapeutic strategy. The polyamidoamine (PAMAM)-polyethylene glycol (PEG) complex was then conjugated with the AS1411 aptamer and confirmed by atomic-force microscopy (AFM) and Fourier transform infrared spectroscopy (FTIR) .In this study, we show that the conjugated PAMAM-PEG-APTAS1411 complex dramatically increased PAMAM-PEG-5-FU uptake by MKN45 gastric cancer cells. We also demonstrated both the stability of the nanoparticle-5-FU-APTAS1411 complex, by thin layer chromatography (TLC), and an increase in 5-fluorouracil (5-FU) accumulation in the vicinity of cancerous tumors. This smart drug delivery system is capable of effectively transferring 5-FU to MKN45 gastric cancer cells in consistent and without toxic effects.

Evaluation of Nanocarrier Targeted Drug Delivery of Capecitabine-PAMAM Dendrimer Complex in a Mice Colorectal Cancer Model.

Capecitabine, an effective anticancer drug in colorectal cancer chemotherapy, may create adverse side effects on healthy tissues. In the present study, we first induced colon adenocarcinoma with azoxymethane, a carcinogen agent, and then investigated the potentiality of polyamidoamine (PAMAM) dendrimer to improve capecitabine therapeutic index and decrease its adverse side effects on healthy tissues like liver and bone marrow. Other variables such as nanoparticle concentrations have also been investigated. Drug loading concentration (DLC) and encapsulation efficiency (EE) were calculated for capecitabine/dendrimer complex. Experimental results showed an increase in DLC percentage resulted from elevated capecitabine/dendrimer ratio. Capecitabine/dendrimer complex could reduce tumor size and adverse side effects in comparison with free capecitabine form.

Pelargonidin improves memory deficit in amyloid ß25-35 rat model of Alzheimer's disease by inhibition of glial activation, cholinesterase, and oxidative stress.

Alzheimer's disease (AD) is a multifactorial disorder with devastating outcomes and few mostly palliative available therapeutic strategies. Pelargonidin (Pel), an anthocyanin compound, is an estrogen receptor agonist with lower side effects versus estrogen. This study examined neuroprotective effect of Pel on intrahippocampal amyloid ß25-35 (Aß) rat model of AD. Rats were divided into groups of sham, Aß, and Pel-pretreated Aß (10mg/kg; p.o.). Animals underwent Morris water maze (MWM) test in addition to measurement of hippocampal oxidative stress, acetylcholinesterase (AChE) activity, glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS). Pel pretreatment of Aß group significantly improved escape latency and distance swum in MWM versus Aß group and attenuated hippocampal malondialdehyde (MDA) and increased catalase activity with no significant change of nitrite. Meanwhile, Pel improved hippocampal AChE activity and lowered GFAP level with no significant change of iNOS. Our results suggest that Pel could improve Aß25-35-induced memory deficit through mitigation of oxidative stress, cholinergic dysfunction, and astrocyte reaction.

Pelargonidin Improves Passive Avoidance Task Performance in a Rat Amyloid Beta25-35 Model of Alzheimer's Disease Via Estrogen Receptor Independent Pathways.

Alzheimer's disease (AD) is a disorder with multiple pathophysiological causes, destructive outcomes, and no available definitive cure. Pelargonidin (Pel), an anthocyanin derivative, is an estrogen receptor agonist with little estrogen side effects. This study was designed to assess Pel memory enhancing effects on the a rat Amyloid Beta25-35 (Aß) intrahippocampal microinjections model of AD in the passive avoidance task performance paradigm and further evaluate the potential estrogen receptor role on the memory-evoking compound. Equally divided rats were assigned to 5 groups of sham, Aß intrahippocampal microinjected, Pel pretreated (10 mg/kg; P.O), α estrogen antagonist intra-cerebrovascular (i.c.v.) microinjected, and ß estrogen antagonist (i.c.v) microinjected animals. Intrahippocampal microinjections of Aß were adopted to provoke AD model. Passive avoidance task test was also used to assess memory performance. Pel pretreatment prior to Aß microinjections significantly improved step-through latency (P<0.001) in passive avoidance test. In α and ß estrogen, antagonists received animals, passive avoidance task performance was not statistically changed (P=0.11 & P=0.41 respectively) compared to Pel pretreated and sham animals. Our results depicted that Pel improves Aß induced memory dysfunction in passive avoidance test performance through estrogen receptor independently related pathways.

Effects of exercise training together with tamoxifen in reducing mammary tumor burden in mice: Possible underlying pathway of miR-21.

Exercise training has an anti-tumor effect and can reduce tumor growth; however, the exact underlying mechanisms of its protective effects are still obscure. MicroRNA (miR)-21 is a predictor in cancer survival, and has a potential use as an indicator of therapeutic outcome in breast malignancies. Forty-eight female BALB/c mice were equally divided into six groups to investigate the effects of interval exercise training with tamoxifen on miR-21 expression and its possible assumed mechanisms in an estrogen receptor-positive breast cancer model. ELISA, immunohistochemistry, western blot, qRT-PCR assays were performed at the end of the study. Tumor size was significantly declined in exercise training and tamoxifen groups compared to tumor group (P<0.05). Expression of miR-21 was significantly down-regulated in trained and tamoxifen treated mice in comparison with tumor group (P<0.05). Exercise training was as effective as tamoxifen treatment in decreasing serum estradiol and ER-α expression (P<0.05). Exercise training and tamoxifen reduced tumor IL-6 levels, NF-kB and STAT3 expressions, and up-regulated TPM1 and PDCD4 expressions (P<0.05). Both exercise and tamoxifen had synergistic effects in reducing miR-21 and Bcl-2, and up-regulating PDCD4 expression. Results showed that interval exercise training may reduce mammary tumor burden in mice through possible underlying pathway of miR-21.

Role of low-intensity laser therapy on naloxone-precipitated morphine withdrawal signs in mice: is nitric oxide a possible candidate mediator?

In the present study, the potential involvement of nitric oxide (NO) system in attenuating effects of low-intensity laser therapy (LILT) on naloxone-induced morphine withdrawal signs was evaluated. A hundred mice were rendered morphine-dependent using three escalating doses of morphine sulfate during three consecutive days. After the last dose on day 4, animals were given naloxone HCl (2 mg/kg s.c) to induce withdrawal signs. The effects of LILT (12.5 J/cm(2)) and L-NG-nitroarginine methyl ester (L-NAME) (10, 20, 50, and 100 mg/kg) and their coadministration on escape jump count and stool weight as typical withdrawal signs were assessed. LILT and L-NAME (20, 50, and 100 mg/kg) per se significantly decreased escape jump count and stool weight in morphine-dependent naloxone-treated mice (p < 0.01). Coadministration of LILT and L-NAME (20, 50, and 100 mg/kg) also reduced escape jump and stool weight (p < 0.05) but with no synergetic or additive response. Here, LILT at this fluence may show its maximal effects on NO and therefore no noticeable effects appeared during coadministration use. Moreover, LILT and L-NAME follow the same track of changes in escape jump and stool weight. Conceivably, it seems that LILT acts partly via NO system, but the exact path is still obscure and rather intricate. The precise mechanisms need to be clarified.

Trend of blood cholesterol level in Iran: results of four national surveys during 1991-2008.

Trends in cholesterol level of different populations have been investigated in several studies. This study is conducted to determine the trend of cholesterol level of Iranian adults from 1990 to 2007. Data on cholesterol measurements of four national health surveys that have been carried out in Iran used in this study. Cholesterol level of 12728 adults aged 25-64 were measured in 1990-1 survey. Also in 1999, 2005, and 2007 surveys, blood cholesterol level of 18398, 52344 and 19630 have been sampled, respectively. The median of cholesterol were modeled with age for men and women separately for the four surveys using fractional polynomials. Then, trends in the median of cholesterol across these four surveys were studied. The analysis of cholesterol data over four national health surveys showed that the change in males' cholesterol level had a decreasing trend. This decreasing trend was more pronounced in ages younger than 45 years. However, the medians of cholesterol of females during 16 years of four national surveys had a varying trend. It was decreasing in ages younger than 45; but increasing in ages over 45 years. The median of the cholesterol level of males and females in 2005 survey was on average about 10 mg/dl higher in comparison with the other surveys. Our findings showed that the pattern of trend in cholesterol level of Iranian men and women adults have a considerable difference with those of the other developing and developed countries.

Fumonisin B1 contamination of cereals and risk of esophageal cancer in a high risk area in northeastern Iran.

INTRODUCTION: Fumonisin B1 (FB1) is a toxic and carcinogenic mycotoxin produced in cereals due to fungal infection. This study was conducted to determine FB1 contamination of rice and corn samples and its relationship with the rate of esophageal cancer (EC) in a high risk area in northeastern Iran. METHODS: In total, 66 rice and 66 corn samples were collected from 22 geographical subdivisions of Golestan province of Iran. The levels of FB1 were measured for each subdivision by thin layer and high pressure liquid chromatographies. The mean level of FB1 and the proportions of FB1 contaminated samples were compared between low and high EC-risk areas of the province. RESULTS: The mean of FB1 levels in corn and rice samples were 223.6 and 21.6 µg/g, respectively. FB1 contamination was found in 50% and 40.9% of corn and rice samples, respectively. FB1 level was significantly higher in rice samples obtained from high EC-risk area (43.8 µg/g) than those obtained from low risk area (8.93 µg/g) (p-value=0.01). The proportion of FB1 contaminated rice samples was also significantly greater in high (75%) than low (21.4%) EC-risk areas (p-value=0.02). CONCLUSION: We found high levels of FB1 contamination in corn and rice samples from Golestan province of Iran, with a significant positive relationship between FB1 contamination in rice and the risk of EC. Therefore, fumonisin contamination in commonly used staple foods, especially rice, may be considered as a potential risk factor for EC in this high risk region.

Impact of fumonisin B1 on the production of inflammatory cytokines by gastric and colon cell lines.

Fumonisins, a family of mycotoxins, are mainly toxic and carcinogenic. The present study was carried out to evaluate fumonisin B1 (FB1) effects on the production of inflammatory cytokines by gastric and colon cell lines. The study was performed on two cell lines under in vitro condition, including gastric epithelial cell line (AGS) and human colon adenocarcinoma cell line (SW742). Lipopolysaccharide (LPS) was used for inflammatory cytokine induction. The culture medium was supplemented with 4.5-72 mg/l of FB1 for 72 h before cell induction. The supernatants were harvested 24 h after the induction and measured for cytokines by using enzyme-linked immunosorbent assay.FB1 induced a dose-dependent increase in the production of tumor necrosis factor-α and interleukin-1ß in both AGS and SW742 cell lines. This increase was statistically significant with concentration of FB1 between 9 and 72 mg/l (P < 0.05). FB1 also induced a dose-dependent decrease in interleukin-8 production. This decrease was seen in both cell lines and showed a statistical significance with FB1 concentration (P < 0.05).The results show that FB1 increases inflammatory cytokines production by various gastric and intestinal cells. This effect in the long run can possibly be the basis for the occurrence or development of inflammation and subsequent atrophy in the above-mentioned tissues.

Oxytocin protects cardiomyocytes from apoptosis induced by ischemia-reperfusion in rat heart: role of mitochondrial ATP-dependent potassium channel and permeability transition pore.

The current study examines the protective effect of oxytocin (OT) on cardiomyocyte apoptosis modulated by mitochondrial ATP-dependent potassium (mitoKATP) channel and permeability transition pore (mPTP) in the preconditioned myocardium of anesthetized rats. Eighty rats were equally divided into eight groups. The hearts of all animals except for the sham group were subjected to 25 min ischemia and 120 min reperfusion. Oxytocin, 5-hydroxydeconoate (5-HD), a specific inhibitor of the mitoKATP channel, and atractyloside (ATRC), an mPTP opener, were used prior to ischemia. Hemodynamic parameters were recorded throughout the experiment. Evaluations were made by infarct size, plasma lactate dehydrogenase level (LDH), transmission electron microscopy (TEM) and immunohistochemistry studies. OT prevented mean arterial pressure drop during early phase of ischemia and reperfusion. Treatment with OT before IR induction normalizes cardiomyocytes both in light microscopy and TEM observations. In addition, OT significantly reduced TUNEL- and increased Bcl-2-labeled positive cell number relative to IR (p<0.05). However, 5HD or ATRC inhibited the protective effects of OT on cardiomyocytes damaged by IR (p<0.05). Ultrastructural changes including extensive myofibril loss, sarcolemmal disruption and mitochondrial swelling due to amorphous dens bodies indicate necrosis induction in 5HD and ATRC as well as in IR groups. Restoration of immunohistochemistry parameters and protection against IR-induced ultrastructural changes confirm OT cardioprotective effects via mitoKATP channel and mPTP modulation in apoptosis induced by ischemia-reperfusion.

Effect of DETA-NONOate and papaverine on vasodilation of human internal mammary artery.

In this study, the relaxatory effect of DETA-NONOate is compared with that of papaverine on isolated human internal mammary artery. We investigated the inhibitory effects of DETA-NONOate and papaverine on phenylephrine-induced contractile response in internal mammary artery segments. The internal mammary artery segments, taken from methodologically matched patients who underwent coronary artery bypass grafting, were prepared, placed in an organ bath, and contracted with phenylephrine (10(-9) to 10(-4) mol/L) to investigate their relaxatory response to DETA-NONOate or papaverine. Phenylephrine dose-response contraction was obtained after 1, 2, and 3 h in segments pre-incubated with DETA-NONOate or papaverine for 30 min. The EC50 that presented for internal mammary artery segments incubated with DETA-NONOate was 3.523 ± 1.2696 × 10(-7) mol/L, and for papaverine was 3.467 ± 1.2145 × 10(-6) mol/L. In segments pre-incubated with DETA-NONOate, the contractile response to phenylephrine was suppressed in the first 2 h post-incubation, compared with control responsive groups (p < 0.05), but this inhibition was revoked after 3 h post-incubation. We showed that DETA-NONOate has a more significant relaxative effect by comparison with papaverine; moreover, continuous and long-lasting nitric oxide production by DETA-NONOate might be of great importance for the outcome from coronary artery bypass grafting, when internal mammary artery is used as a conduit.

The effect of teucrium polium honey on the wound healing and tensile strength in rat.

OBJECTIVES: Wound healing represents a dynamic physiological process influenced by many factors. The aim of the present study was to evaluate the effects of Teucrium polium honey on the wound healing and tensile strength in rat. MATERIALS AND METHODS: Thirty-six Sprague-Dawley rats were randomly divided into four equal (n= 9) treatment and control groups. Two full-thickness wounds were made over the dorsal thoracic region according to the incision and excision models. Animals were treated with topical Teucrium polium honey twice a day post surgery until complete healing was achieved. Histopathology and tensiometry were then studied. RESULTS: The wound healing process occurred faster in the incision model than excision ones (P< 0.05). Teucrium polium honey promoted wound contraction, closure time and tensile strength (P< 0.05). Histopathological study also showed relative epithelial proliferation, improved angiogenesis granulation, and fibrous connective tissue in Teucrium polium honey treated animals. CONCLUSION: The present study demonstrates that Teucrium polium honey can accelerate wound healing as well as tensile strength in rat skin wounds.

Attenuation of morphine withdrawal signs by low level laser therapy in rats.

In the present study, the effects of low-intensity laser therapy (LILT) on naloxone-induced withdrawal signs of morphine-dependent rats were examined. Low-intensity lasers with a power density of 12.5J/cm(2) have been used by a Ga-Al-As laser. One-way ANOVA showed that the LILT which applied immediately or 15min prior to naloxone injection significantly decreased total withdrawal score (TWS). These results suggest that LILT prior to naloxone injection attenuates the expression of withdrawal signs in morphine-dependent rats. Further studies may elucidate the likely role of LILT in clinical management of opioid withdrawal syndrome.

Cardiovascular response to renin substrate microinjection into the central nucleus of the amygdala of rats.

Central nucleus of the amygdala is involved in cardiovascular regulation. Although most components of the renin-angiotensin system have been found to be distributed in amygdala, renin expression in brain has remained controversial. This work was undertaken to elucidate the extent of renin presence in this nucleus. A cannula was implanted bilaterally into the central nucleus of the amygdala. Mean arterial pressure and heart rate were directly measured via indwelling femoral artery cannula post bilateral intra central nucleus of the amygdala microinjection of renin substrate. Renin substrate microinjection dose-dependently increased mean arterial pressure and heart rate, whereas captopril, saralasin and losartan pretreatment inhibited these effects. The results suggest the presence of local renin or similar proteases in this nucleus.

Attenuation of morphine withdrawal signs by a D1 receptor agonist in the locus coeruleus of rats.

In the present study, the effects of intra-locus coeruleus injection of a dopamine D(1) receptor agonist (SKF38393) on naloxone-induced withdrawal signs of morphine-dependent rats were examined. Twenty different withdrawal signs were assessed. The total withdrawal score was calculated and used as an index of withdrawal intensity for comparison. The D(1) agonist and antagonist were injected 15 and 30 min prior to expression of naloxone-induced withdrawal signs, respectively. SKF38393 (2 and 4 microg/site) decreased while SCH23390 (a D(1) antagonist) had no effect on the total withdrawal score. On the other hand, SCH23390 (25 ng/site) reversed the SKF38393 effect. It may be concluded that activation of dopamine D(1) receptors in the locus coeruleus attenuates naloxone-induced withdrawal.

Relaxatory effect of magnesium on mesenteric vascular beds differs from normal and streptozotocin induced diabetic rats.

Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of diabetes complications. Previous studies have shown that magnesium decreases basal tone in normal isolated aortic rings and reduces phenylephrine-induced contraction. The mechanism of this magnesium action is not very well known. The present study was designed to determine the role of endothelium and nitric oxide in magnesium sulfate-induced vasorelaxation in diabetic rat vessels. Diabetes was induced by a single tail injection of streptozotocin. Eight weeks later, superior mesenteric arteries of control and diabetic animals were isolated and perfused according to the McGregor method. Prepared vascular beds were constricted with phenylephrine to induce 70-75% of maximal constriction. Magnesium sulfate at concentrations of 0.001 M to 0.1 M was added into the medium and perfusion pressure was then recorded. Mesenteric bed baseline perfusion pressure in intact and denuded endothelium of diabetic groups was higher than controls. In all groups, relaxant response to magnesium in mesenteric bed was attenuated after endothelium removal, but a relaxatory effect appears at high concentration. In the presence of N (omega)-nitro-L-arginine methyl ester (L-NAME), magnesium-induced relaxation was significantly suppressed in intact mesenteric bed of control animals but in diabetics, the relaxant response was slightly inhibited. From the results of this study, it can be concluded that magnesium-induced endothelium dependent and endothelium independent vasorelaxation are mediated by nitric oxide in control rats while in diabetic animals other mechanisms may be involved.

Oral magnesium administration prevents vascular complications in STZ-diabetic rats.

Vascular disease is one of the complicating features of diabetes mellitus. Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of diabetes complications. Several studies have indicated that hypertension in diabetic patients is an independent altered reaction of blood vessels to neurotransmitters and circulating hormones. Since magnesium has been proposed to decrease vascular sensitivity to vasoconstrictor agents, the present study was designed to determine whether chronic magnesium sulfate administration could prevent vascular complications of STZ-induced diabetes in rats. The animals were divided into six groups: two groups served as controls and received tap water for 8 weeks, while in the other four groups, made diabetic with a single IV injection of 40 mg/kg STZ, two groups treated with magnesium sulfate (10 g/L) added to the drinking water, and the other two groups received tap water only. After 8 weeks, in 3 groups (control, diabetic and Mg-treated), left common carotid artery was cannulated for continuous recording of blood pressure. All animals in these groups were decapitated and blood samples were drawn for glucose, Ca and Mg measurements. In the 3 remaining groups (again divided into control, diabetic and Mg-treated), the mesenteric vascular bed was perfused according to the McGregor method, and descending thoracic aortas were used for measurement of elasticity. In diabetic rats, plasma glucose was significantly increased and plasma magnesium was significantly decreased compared to controls and Mg-treated animals. Although plasma magnesium of Mg-treated animals increased significantly, it failed to reach to the magnesium level of the control group. Ca/Mg ratio was also increased compared to the control and Mg-treated animals. Mean arterial blood pressure in diabetics was significantly higher than control and Mg-treated rats. Similarly, there was a significant difference in mean arterial blood pressure of Mg-treated rats compared to control animals. Baseline perfusion pressure of diabetic group was significantly higher than control and Mg-treated groups with intact and denuded endothelium. Magnesium sulfate treatment decreased mean perfusion pressure of mesenteric vascular bed in intact and denuded endothelium in comparison with non-treated diabetic rats. There was a significant increase in passive tension in the aorta of diabetic rats compared to control and Mg-treated rats. However, there was no significant difference between Mg-treated and control rats. From the results of this study it may be concluded that magnesium could control STZ-induced diabetes and prevent its vascular complications.