Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension.

Aims: Activation of the renin-angiotensin system (RAS), renal oxidative stress and inflammation are constantly present in experimental hypertension. Nitric oxide (NO) inhibition with N(w)-nitro-L-arginine methyl ester (L-NAME) has previously been reported to produce hypertension, increased expression of Angiotensin II (Ang II) and renal dysfunction. The use of Losartan, an Ang II type 1 receptor (AT1R) antagonist has proven to be effective reducing hypertension and renal damage; however, the mechanism by which AT1R blockade reduced kidney injury and normalizes blood pressure in this experimental model is still complete unknown.

Longterm melatonin administration alleviates paraquat mediated oxidative stress in Drosophila melanogaster.

We investigated the effect of melatonin (MEL) in the activities of cytosolic superoxide dismutase (SOD) and catalase as well as in the levels of H2O2 and mitochondrial malondialdehyde (MDA) in paraquat-intoxicated Drosophila melanogaster. Paraquat (40 mM) was administrated for 36 h. Three groups of flies intoxicated with paraquat were used: PQ (exposed during 36h to paraquat), PQ-MEL (exposed during 36h to paraquat and then treated with MEL [0.

Minocycline increases the activity of superoxide dismutase and reduces the concentration of nitric oxide, hydrogen peroxide and mitochondrial malondialdehyde in manganese treated Drosophila melanogaster.

The toxicity caused by high concentrations of manganese (Mn) could be due to a production of free radicals. Minocycline is an effective antioxidant with a high potential to capture free radicals. We investigated the effect of minocycline in the activities of superoxide dismutase (SOD) and catalase, and in the concentrations of nitric oxide (NO), hydrogen peroxide (H2O2) and mitochondrial malondialdehyde (MDA) in manganese-treated Drosophila melanogaster.

Minocycline, but not ascorbic acid, increases motor activity and extends the life span of Drosophila melanogaster.

In the present study we compared the effects of minocycline and ascorbic acid in the life span, motor activity and lipid peroxidation of Drosophila melanogaster, in an effort to find a substance capable of providing protection against oxidative stress in aging. In the flies treated with minocycline a very significant increase in the life span (101 +/- 1.33 days) was observed when compared to those treated with ascorbic acid and controls (42.

[Copper intoxication decreases lifespan and induces neurologic alterations in Drosophila melanogaster].

Wilson disease is a hereditary disorder caused by mutations of the ATP7B gene, which leads to intoxication with copper as a result of an unbalance of copper homeostasis. The clinical manifestations resulting from this intoxication are related to the affectation of liver and the encephalon in most cases. Several animal models are currently available for the study of the malady.

The life span of Drosophila melanogaster is affected by melatonin and thioctic acid.

Aging and reduced longevity are due in part to the action of free radicals (FR). Melatonin (Mel) and thioctic acid (TA) are effective in protecting against the damage caused by FR. In this study, the effect of Mel and TA on the life cycle of Drosophila melanogaster was determined.

Overexpression of HGF transgene attenuates renal inflammatory mediators, Na(+)-ATPase activity and hypertension in spontaneously hypertensive rats.

Renal inflammation and oxidative stress are constantly present in experimental hypertension. Since the spontaneously hypertensive rat (SHR) has reduced levels of hepatocyte growth factor (HGF), which suppresses the activation of the proinflammatory nuclear transcription factor kappa B (NF-κB), we speculated that HGF deficiency could play a key role in the pathogenesis of hypertension in the SHR. To test this hypothesis we increased HGF in the SHR by HGF gene delivery.

Experimental depression induces renal oxidative stress in rats.

Depression has been associated to inflammatory and oxidative events. Previous report has shown renal oxidative stress in patients with depression. In order to analyze if depressive status is related to renal oxidative and inflammatory events, Sprague Dawley rats were submitted to forced swimming test (FST) and the renal oxidative metabolism, monocyte-macrophage infiltration and Angiotensin II (Ang II) expression were determined.

Forced swimming test decreases chemotactic responsiveness and expression of CD11a in rat monocytes.

Objectives: Previous reports have shown that the depressive status in humans and experimental animals is associated with decreased immune response. Since monocyte chemotaxis and expression of CD11a are pivotal mechanisms in immune response, impairment of these events could explain the diminished immune response in depression.

Methods: To test this, rats were submitted to the forced swimming test (FST) for 3 and 15 days.

Structural and ultrastructural analysis of cerebral cortex, cerebellum, and hypothalamus from diabetic rats.

Autonomic and peripheral neuropathies are well-described complications in diabetes. Diabetes mellitus is also associated to central nervous system damage. This little-known complication is characterized by impairment of brain functions and electrophysiological changes associated with neurochemical and structural abnormalities.

Depressive status does not alter renal oxidative and immunological parameters during early diabetic nephropathy in rats.

Depression is frequently observed among patients with diabetes and depressive status has been associated to activation of inflammatory processes, suggesting a role of depression in the inflammatory events observed in diabetes. To test that proposal, it was studied the effect of depression induced by forced swimming test (FST) on the evolution of early diabetic nephropathy. Diabetes was induced by streptozotocin injection.

Forced swimming test increases superoxide anion positive cells and angiotensin II positive cells in the cerebrum and cerebellum of the rat.

Situations of stress are capable of inducing depression and oxidative stress in the brain. Previous reports have shown that angiotensin II (Ang II) induces the production of superoxide anion (O(2)(-)), and impairment of endothelial function in cerebral microvessels in vivo. Substances that reduce angiotensin functions may be important in the treatment of depression.

Stress-induced muscle and cutaneous hyperalgesia: differential effect of milnacipran.

We previously demonstrated that repeated swim stress produces long-term cutaneous hyperalgesia in rats. We have now determined the effect of stress upon muscle nociception and the anti-nociceptive efficacy of the norepinephrine-serotonin reuptake inhibitor, milnacipran (MIL) in this model. Rats were subjected to either 10-20 min daily sessions of forced swimming (FS) for 3 days, or sham swimming (SS) or control (CT).

Role of mu-opioid and NMDA receptors in the development and maintenance of repeated swim stress-induced thermal hyperalgesia.

Repeated exposure to swimming stress induces a long-lasting hyperalgesia in the rat by mechanisms to be elucidated. Since opioid and glutamate neurotransmitter systems modulate pain, we now evaluated the effect of pharmacological blockade of opioid and glutamate receptors subtypes on forced swimming stress-induced hyperalgesia. Male rats were daily subjected to 10-20 min of forced or sham swimming for 3 days and thermal nociception was estimated twice, before each behavioral conditioning and 24 h after the last, using hot plate test.

Repeated swim stress increases pain-induced expression of c-Fos in the rat lumbar cord.

We have previously demonstrated that repeated swim stress produces a long-lasting cutaneous hyperalgesia in rats. We have now looked at c-Fos expression in the spinal lumbar cord of male Sprague-Dawley rats subjected to 10-20 min daily sessions of forced swimming for 3 consecutive days. Control rats were subjected to sham swimming or were completely naive.

Long-lasting delayed hyperalgesia after subchronic swim stress.

Rats subjected to an inescapable subchronic stress, consisting of 10-20 min of forced swimming for 3 days, showed a thermal hyperalgesia and an enhanced nociceptive behavior to the subcutaneous administration of formalin 24 and 48 h, respectively, after the last swim session. Hyperalgesia to thermal and chemical stimulants was still present 8 and 9 days after the last swim session, respectively. Chemical, but not thermal, nociception was negatively correlated with the swim effort or struggle times during the last swim session.

Opposite modulation of capsaicin-evoked substance P release by glutamate receptors.

Substance P and glutamate are present in primary afferent C-fibers and play important roles in persistent inflammatory and neuropathic pain. In the present study, we have examined whether activation of different glutamate receptor subtypes modulates the release of substance P evoked by the C-fiber selective stimulant capsaicin (1 microM) from rat trigeminal nucleus slices. The selective NMDA glutamate receptor agonist L-CCG-IV (1-10 microM) enhanced capsaicin-evoked substance P release about 100%.

Multiphasic morphine modulation of substance P release from capsaicin-sensitive primary afferent fibers.

Morphine produces a multiphasic modulation of K+-evoked substance P release from trigeminal slices and dorsal root ganglion neurons in culture. We now found that the C-fiber stimulant, capsaicin (1 microM), evoked release of substance P that was inhibited, enhanced and inhibited by 0.1 nM, 1 microM, and 10 microM morphine, respectively.

[A proposal for application and scoring of the Clock Drawing Test in Alzheimer's disease].

Introduction: The Clock Drawing Test (CDT) has been used in recent years as a simple neuropsychological instrument to assess cognitive deterioration associated with dementia, even though uniform operative criteria with respect to its application and scoring have not been established.

Objective: To present application normatives and establish the most relevant psychometric criteria of the CDT in a sample of healthy subjects (HS) and patients with Alzheimer's disease (AD).

Patients And Methods: 56 patients were selected of which 35 were female and 21 were male.

Decrease in spontaneous motor activity and in brain lipid peroxidation in manganese and melatonin treated mice.

In the present study, we have evaluated whether melatonin (MEL) modulates Mn-induced decrease in spontaneous motor activity (SMA) and lipid peroxidation, estimated as malondialdehyde (MDA) formation, in several brain regions. In mice treated with manganese a decrease in SMA after 2 weeks of treatment was observed. In the group treated with Mn+MEL a significant greater reduction in SMA was detected at 4 weeks.

Dynorphin A increases substance P release from trigeminal primary afferent C-fibers.

Dynorphin A-(1-17) has been found to produce spinal antianalgesia and allodynia. Thus, we studied whether dynorphin A-(1-17) modulates substance P release evoked by the C-fiber-selective stimulant capsaicin (1 microM) from trigeminal nucleus caudalis slices. Very low concentrations of dynorphin A-(1-17) (0.

[Genotype and phenotype of apolipoprotein E in patients with Alzheimer's disease in Castille and Leon].

We determined the variants of the apolipoprotein E (apo-E) in a sample taken from a castellano-leonesa population with Alzheimer's disease (AD). The prevalence of the allele E-4 is 0.33 in AD and 0.

Delayed-onset dystonia in patients with antecedents of perinatal asphyxia.

We report 27 cases of delayed-onset dystonia in patients with antecendents of perinatal asphyxia after excluding other possible causes of dystonia. The patients were 16 males and 11 females (mean +/- SD age at onset of dystonia = 13.0 +/- 9.