Ventrolateral medulla mechanisms involved in cardiorespiratory responses to central chemoreceptor activation in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Purinergic mechanisms of lateral parabrachial nucleus facilitate sodium depletion-induced NaCl intake

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Hypothalamic disconnection caudal to paraventricular nucleus affects cardiovascular and drinking responses to central angiotensin II and carbachol

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Chemosensory control by commissural nucleus of the solitary tract in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Commissural NTS lesions enhance the pressor response to central cholinergic and adrenergic activation

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Influence of different light sources and photo-activation methods on degree of conversion and polymerization shrinkage of a nanocomposite resin

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Reduced allergic lung inflammation in rats following formaldehyde exposure: Long-term effects on multiple effector systems

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Involvement of the Central Nervous System in the Salivary Secretion Induced by Pilocarpine in Rats

The effect in rats of an anteroventral third ventricle (AV3V) electrolytic lesion on salivary secretion induced by intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) injection of a cholinergic agonist (pilocarpine) was investigated. Sham- or AV3V-lesioned rats anesthetized with urethane and with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The amount of salivary secretion was studied over a seven-minute period after i.c.v. or i.p. injection of pilocarpine. In sham-operated rats, i.p. injection of pilocarpine (1 mg/kg b.w.) (after 6 h, 2, 7, and 15 days) produced salivary secretion (486 +/- 21, 778 +/- 85, 630 +/- 50, and 560 +/- 55 mg/7 min, respectively). This effect was reduced 6 h, 2, and 7 days after an AV3V lesion (142 +/- 22, 113 +/- 32, and 290 +/- 62 mg/7 min, respectively), but not 15 days after an AV3V lesion (516 +/- 19 mg/7 min). I.c.v. injection of pilocarpine (120 mug in 1 muL), in sham-operated rats after 6 h, 2, 7, and 15 days also produced salivary secretion (443 +/- 20, 417 +/- 81, 496 +/- 14, and 427 +/- 47 mg/7 min, respectively). The effects of i.c.v. pilocarpine were also reduced 6 h, 2, and 7 days after an AV3V lesion (143 +/- 19, 273 +/- 14, and 322 +/- 17 mg/7 min, respectively), but not after 15 days (450 +/- 28 mg/7 min). The results demonstrate that the central nervous system, and particularly the AV3V region, is important for the effect of pilocarpine on salivary secretion in rats. Moreover, they suggest that activation of central pathways may play an important part in the salivary secretion to peripheral pilocarpine in rats.

THE ROLE OF ANGIOTENSIN AT1 RECEPTORS IN THE DIURETIC, NATRIURETIC, KALIURETIC AND BLOOD-PRESSURE RESPONSES INDUCED BY ANGIOTENSIN-II ACTIVATION OF THE MEDIAN PREOPTIC NUCLEUS IN CONSCIOUS RATS

We determined the effects of two classical angiotensin II (ANG II) antagonists, [Sar(1), Ala(8)]-ANG II and [Sar(1), Thr(8)]-ANG II, and losartan (a nonpeptide and selective antagonist for the AT 1 angiotensin receptors) on diuresis, natriuresis, kaliuresis and arterial blood pressure induced by ANG II administration into the median preoptic nucleus (MnPO) of male Holtzman rats weighing 250-300 g. Urine was collected in rats submitted to a water load (5% body weight) by gastric gavage, followed by a second water load (5% body weight) 1 h later. The volume of the drug solutions injected was 0.5 mu l over 10-15 s. Pre-treatment with [Sar(1), Ala(8)]-ANG II (12 rats) and [Sar(1), Thr(8)]-ANG II (9 rats), at the dose of 60 ng reduced (13.7 +/- 1.0 vs 11.0 +/- 1.0 and 10.7 +/- 1.2, respectively), whereas losartan (14 rats) at the dose of 160 ng totally blocked (13.7 +/- 1.0 vs 7.6 +/- 1.5) the urine excretion induced by injection of 12 ng of ANG II (14 rats). [Sar(1), Ala(8)]-ANG II impaired Na+ excretion (193 +/- 16 vs 120 +/- 19): whereas [Sar(1), Thr(8)]-ANG II and losartan blocked Na+ excretion (193 +/- 16 vs 77 +/- 15 and 100 +/- 12, respectively) induced by ANG II. Similar effects induced by ANG II on K+ excretion were observed with [Sar(1), Ala(8)]-ANG II, [Sar(1), Thr(8)]-ANG II, and losartan pretreatment (133 +/- 18 vs 108 +/- 11, 80 +/- 12, and 82 +/- 15, respectively). The same doses as above of [Sar(1), Ala(8)]-ANG II (8 rats), [Sar(1), Thr(8)]-ANG II (8 rats). and losartan (9 rats) blocked the increase in the arterial blood pressure induced by 12 ng of ANG II (12 rats) (32 +/- 4 ru 4 +/- 2, 3.5 +/- 1, and 2 +/- 1: respectively. The results indicate that the AT1 receptor subtype participates in the increases of diuresis, natriuresis. kaliuresis and arterial blood pressure induced by the administration of ANG II into the MnPO.

AV3V-LESION IMPAIRS RESPONSES INDUCED BY CHOLINERGIC ACTIVATION OF SFO IN RATS

This study was performed to investigate the effect of lesion of the anteroventral third ventricle (AV3V) region on the pressor, bradycardic, dipsogenic, natriuretic, kaliuretic, and antidiuretic responses induced by cholinergic activation of the subfornical organ (SFO) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with a stainless steel cannula directly into the SFO. Microinjection of the cholinergic agonist carbachol (2 nmol) into the SFO of sham rats induced natriuresis (563 +/- 70 mueq/120 min), kaliuresis (205 +/- 13 mueq/120 min), antidiuresis (10.4 +/- 0.5 ml/120 min), water intake (9.3 +/-1.4 ml/h), bradycardia (-42 +/- 11 beats/min), and increased mean arterial pressure (53 +/- 3 mmHg). In AV3V-lesioned rats (1-5 and 14-18 days), there was a reduction of natriuresis (23 +/-11 and 105 +/- 26 mueq/120 min, respectively), kaliuresis (92 +/- 16 and 100 +/- 17 mueq/120 min), water intake (2.5 +/- 0.9 and 1.8 +/- 1.0 ml/h), and arterial pressure increase (17 +/- 2 and 16 +/- 2 mmHg) induced by carbachol into the SFO. Increased antidiuresis (6.0 +/- 1.0 and 5.2 +/- 0.7 ml/120 min, respectively) and tachycardia (39 +/- 4 and 15 +/- 12 beats/min) instead of bradycardia were also observed in both groups of AV3V-lesioned rats. These results show that cholinergic activation of the rat SFO produces marked natriuresis and kaliuresis in addition to the well-known pressor and dipsogenic responses. They also show that the AV3V region plays an important role in the cardiovascular, fluid, and electrolytic changes induced by cholinergic activation of the SFO in rats.

Aging behaviour of 25Cr-17Mn high nitrogen duplex stainless steel

The precipitation behaviour of a nickel free stainless steel containing 25% chromium, 17% manganese and 0.54% nitrogen, with duplex ferritic-austenitic microstructure, was studied using several complementary techniques of microstructural analysis after aging heat treatments between 600 and 1 000 degrees C for periods of lime between 15 and 6 000 min. During aging heat treatments, ferrite was decomposed into sigma phase and austenite by a eutectoid reaction, like in the Fe-Cr-Ni duplex stainless steel. Chromium nitride precipitation occurred in austenite, which had a high nitrogen supersaturation. Some peculiar aspects were observed in this austenite during its phase transformations. Chromium nitride precipitation occurred discontinuously in a lamellar morphology, such as pearlite in carbon steels. This kind of precipitation is not an ordinary observation in duplex stainless steels and the high levels of nitrogen in austenite can induce this type of precipitation, which has not been previously reported in duplex stainless steels. After chromium nitride precipitation in austenite, it was also observed sigma phase formation near the cells or colonies of discontinuously precipitated chromium nitride. Sigma phase formation was made possible by the depletion of nitrogen in those regions. Time-temperature-transformation (precipitation) diagrams were determined.

Transcriptional activation of MMP-13 by periodontal pathogenic LPS requires p38 MAP kinase

Matrix metal loprotease-13 (MMP-13) is induced by pro-inflammatory cytokines and increased expression is associated with a number of pathological conditions such as tumor metastasis, osteoarthritis, rheumatoid arthritis and periodontal diseases. MMP-13 gene regulation and the signal transduction pathways activated in response to bacterial LPS are largely unknown. In these studies, the role of the mitogen-activated protein kinase (MAPK) pathways in the regulation of MMP-13 induced by lipopolysaccharide was investigated. Lipopolysaccharide from Escherichia coli and Actinobacillus actinomycetemcomitans significantly (P < 0.05) increased MMP-13 steady-state mRNA (average of 27% and 46% increase, respectively) in murine periodontal ligament fibroblasts. MMP-13 mRNA induction was significantly reduced by inhibition of p38 MAP kinase. Immunoblot analysis indicated that p38 signaling was required for LPS-induced MMP-13 expression. Lipopolysaccharide induced proximal promoter reporter (-660/+32 mMMP-13) gene activity required p38 signaling. Collectively, these results indicate that lipopolysaccharide-induced murine MMP-13 is regulated by p38 signaling through a transcriptional mechanism.

Anxiogenic-like effects induced by NMDA receptor activation are prevented by inhibition of neuronal nitric oxide synthase in the periaqueductal gray in mice

Glutamate-NMDA (N-methyl-D-aspartate) receptor activation within the periaqueductal gray (PAG) leads to antinociceptive, autonomic and behavioral responses characterized as the fear reaction. We have recently demonstrated that the vigorous defensive-like behaviors (e.g. jumping and running) and antinociception induced by intra-PAG injection of N-methyl-D-aspartate (NMDA) were completely blocked by prior infusion of N(omega)-propyl-L-arginine (NPLA), a specific neuronal nitric oxide synthesis (nNOS) enzyme inhibitor, into the same midbrain structure. It remains unclear however, whether the inhibition of nNOS within the mouse PAG changes the anxiety-like behavior per se or the effects of the inhibition of nNOS depend on the suppression of downstream of glutamate-NMDA receptor activation. This study investigated whether intra-PAG infusion of NPLA (i) attenuates anxiety in the elevated plus-maze (EPM) and (ii) antagonizes the anxiogenic-like effects induced by intra-PAG injection of NMDA. Test sessions were videotaped and subsequently scored for conventional indices of anxiety (percentage of open arm entries and percentage of open arm time) and locomotor activity (closed arm entries). Results showed that intra-PAG infusions of NPLA (0.2, 0.4 or 0.8 nmol/0.1 mu l) did not alter significantly any behavioral response in the EPM when compared to control group (Experiment 1). Intra-PAG infusion of NMDA (0 and 0.02 nmol/0.1 mu l; a dose that does not provoke vigorous defensive behaviors per se in mice) significantly reduced open arm exploration, confirming an anxiogenic-like effect (Experiment 2). When injected into the PAG 10 min prior local NMDA injection (0.02 nmol/0.1 mu l), NPLA (0.4 nmol/0.1 mu l) was able to revert the anxiogenic-like effect of glutamate-NMDA receptor activation. Neither intra-PAG infusion of NMDA nor NPLA altered closed arm entries, a widely used measure of locomotor activity in the EPM. These results suggest that intra-PAG nitric oxide synthesis does not play a role on anxiety-like behavior elicited during EPM exposure; however its synthesis is important for the proaversive effects produced by activation of glutamate-NMDA receptors located within this limbic midbrain structure. (C) 2008 Elsevier B.V. All rights reserved.

Pressor, dipsogenic, natriuretic and kaliuretic responses to central carbachol in rats with lesion of the medial septal area

In the present study we investigated the effect of electrolytic lesion of the medial septal area (MSA) on the dipsogenic, natriuretic, kaliuretic and pressor responses elicited by intracerebroventricular (i.c.v.) injection of the cholinergic agonist carbachol. Freely moving rats with sham or MSA lesion (1-7 days and 14-18 days) and a stainless steel cannula implanted into the lateral ventricle were studied. In sham rats, i.c.v. injection of carbachol (7.5 nmol) produced an increase in water intake (10.2 ± 1.5 ml/h), mean arterial pressure (MAP) (35 ± 5 mmHg) and urinary Na+ and K+ excretion (551 ± 83 and 170 ± 17 μEq 120 min, resp.). The pressor (18 ± 3 and 14 ± 4 mmHg, resp.) and natriuretic responses (178 ± 58 and 172 ± 38 μEq 120 min) produced by i.c.v. carbachol in acute or chronic MSA-lesioned rats were reduced. No change was observed in urinary K+ excretion and a reduced water intake (5 ± 1.3 ml/h) was observed only in acute MSA-lesioned rats. These results suggest that the MSA plays an important role for the pressor and natriuretic responses induced by central cholinergic activation in rats. A small influence of this structure on water intake may also be suggested. © 1991.

A new application of humic substances: Activation of supports for invertase immobilization

Invertase was immobilized on aminopropyl silica (APTS-SiO2) activated with humic substances (APTS-SiO2-HS) and on aminopropyl silica activated with glutaraldehyde (APTS-SiO2-GA). The resulting activity of both systems was compared. Humic substances (HS) used for the activation of the silica were extracted from soil of Cananéia, São Paulo State, Brazil, according to the procedure recommended by the International Humic Substances Society. Activity was determined by measuring the rate of formation of reduced sugars using the reaction with dinitrosalicylic acid (DNS). The amount of HS bound on the APTS-SiO2 was equal to 50 mg. The maximum amount of invertase immobilized on APTS-SiO2-HS was 15200 U/g while in the system APTS-SiO2-GA it was 13400 U/g. The experimental enzymatic activity was 3700 and 3300 U/g, for the systems APTS-SiO2-HS and APTS-SiO2-GA, respectively. Considering the increased amount and activity of immobilized enzyme compared with the glutaraldehyde method, it was concluded that this technique opens a new perspective in the preparation of supports for enzyme immobilization employing humic substances. © Springer-Verlag 2000.