Ograniczanie wyników

Czasopisma help
Autorzy help
Lata help
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 20

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  peripheral tissue
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Galanin is a peptide present in the nervous system and peripheral tissues which exerts a broad range of physiological functions. The influence of centrally administered galanin (Gal; 100 pM i.c.v.) on arginine vasopressin (AVP) and oxytocin (OT) content in the hypothalamus and neurohypophysis as well as on their blood plasma concentration was estimated in male Wistar rats drinking ad libitum 2% solution of natrium chloride per 48 hours. In euhydrated rats and subsequently applied i.c.v. with Gal a significant fall in the hypothalamic and neurohypophysial content of OT but not AVP was observed, however, without simultaneous changes in these neurohormones blood plasma concentration. On the contrary, i.c.v. injection of Gal to salt-loaded rats caused a marked raise in AVP and OT level in the hypothalamus and neurohypophysis with subsequent diminution of both neurohormones concentration in blood plasma. These results suggest that in euhydrated rats Gal has an inhibitory influence on the biosynthesis as well as axonal transport of OT, but not AVP. On the contrary, in salt-loaded rats galanin restricts secretion of both neurohormones into the systemic circulation.
The aims of this study were to evaluate the influence of an extremely low-frequency electromagnetic field (ELF-EMF) on [³H]glucose uptake in the peripheral tissues and organs of rats. Rats were exposed to EL F-EM F (frequency-10 Hz, induction -1.8-3.8 mT) one hour daily for 14 consecutive days. Control animals were sham exposed. On the 15th day (24 hours after last exposure) rats were injected with D-[³H]-6-glucose 500μCi/kg IP. Fifteen minutes later animals were sacrificed by decapitation and peripheral tissues were excised and examined for radioactivity (desintegrations per minute, DPM/100 mg wet tissue weight), which expressed [³H]glucose uptake. In most of the examined tissues and organs, such as liver, kidney, heart muscle, cartilage, connective tissue, tendon and skin, [³H]glucose uptake in EL F-EM F-exposed animals was significantly higher as compared to that in the sham control. Exposure to EL F-EM F did not influence [³H]glucose uptake in the thoracic aorta and the skeletal muscle. It is concluded that ELF-EMF impacts tissue glucose uptake by facilitating glucose transport via cell membranes, dependent and probably also independent of its role in increasing insulin action in insulin-dependent tissues.
The effect of centrally administered galanin (Gal; 100 pM i.c.v.) on the hypothalamo-neurohypophysial storage as well as blood plasma level of vasopressin and oxytocin was estimated in haemorrhaged (1 ml per 100 g b.w.) male Wistar rats. Gal i.c.v. treatment did not alter vasopressin and oxytocin content both in the hypothalamus and neurohypophysis as well as their concentration in blood plasma of not haemorrhaged rats. Haemorrhage decreased the hypothalamic and neurohypophysial vasopressin and oxytocin storage but increased the neurohormones plasma level in animals injected with vehicle solution. During the haemorrhage, the increase in plasma vasopressin and oxytocin was inhibited in rats previously treated i.c.v. with galanin. The hypothalamic and neurohypophysial vasopressin as well as oxytocin content significantly increased in animals treated with galanin and subsequently haemorrhaged. These results suggest that galanin may have a regulatory role in the hypothalamo-neurohypophysial function especially under condition of hypovolemia.
Advances in understanding the functional aspects of leptin in the processes affecting peripheral tissues have brought to the forefront the role of this pluripotent cytokine in the processes of gastric mucosal defense and repair. Here, we report that leptin protects the gastric mucosal cells against ethanol cytotoxicity. We show that ethanol cytotoxicity, characterized by a marked drop in the mucosal cells capacity for NO production, arachidonic acid release and prostaglandin generation, was subject to suppression by leptin. The loss in countering capacity of leptin on the ethanol-induced cytotoxicity was attained with cyclooxygenase inhibitor, indomethacin and nitric oxide synthase (cNOS) inhibitor, L-NAME, as well as PP2, an inhibitor of Src kinase. Indomethacin caused the inhibition in PGE2 generation, pretreatment with L-NAME led to the inhibition in NO production, whereas PP2 exerted the inhibitory effect on leptin-induced changes in NO, arachidonic acid and PGE2. The leptin-induced changes in arachidonic acid release and PGE2 generation were blocked by ERK inhibitor, PD98059, but not by PI3K inhibitor, wortmannin. Moreover, the stimulatory effect of leptin on the mucosal cells cNOS activity was inhibited not only by PP2, but also by Akt inhibitor, SH-5. Our findings demonstrate that leptin protection of gastric mucosa against ethanol cytotoxicity involves Src kinase-mediated bifurcated activation of MAPK/ERK and Akt that leads to up-regulation of the respective prostaglandin and nitric oxide synthase pathways.
8
72%
In addition to the central nervous system, glutamate receptors have been recently identified in a number of peripheral tissues, including adrenals. Pharmacological evidence indicates that adrenal glutamate receptors may be involved in stress response, particularly in catecholamine release. However, possible stress-induced changes at the level of local receptors themselves have not been evaluated yet. This study was aimed to investigate gene expression of N-methyl-D-aspartate (NMDA) receptor subunits (NR1, NR2A, NR2B) in rat adrenal gland under basal and stress conditions, using RT-PCR. NR1 mRNA was found to be present in the adrenal gland, while mRNAs coding for NR2-type subunits failed to be detected in adrenal tissue. The distribution of NR1 mRNA in rat adrenals showed higher concentrations in the adrenal medulla (228%) compared to those in the cortex. Single stress stimulus (immobilization) induced a significant increase of NR1 gene expression in both medullar (by 25%) and cortical (by 66%) regions of the adrenal gland at 24 h, while no changes were observed at 3 h after the stress exposure. It is possible that delayed rise in adrenal NR1 gene expression following stress exposure represents one of the factors by which stress exerts long-term effects on adrenal function at the molecular level.
To determine the susceptibility of developing brain and other tissues to accumulate zinc, rats were exposed to zinc at different periods of ontogeny. For the prenatal group, pregnant Wistar rats received 50 ppm of zinc (ZnSO₄ · 7H₂O) in drinking for the entire duration of pregnancy. On the day of delivery zinc was removed from the drinking water. Another group, dams, received 50 ppm of zinc in drinking water only during the suckling period (from delivery until the 21st day of postnatal life). Their offspring were weaned on the 21st day, at which time zinc was removed from the drinking water. The control group drank tap water only. At 3 weeks after birth, the level of zinc was estimated in the brain, liver, mandibular bone and kidney of offspring from all groups. At 8 weeks after birth 6-[³H]D-glucose (500 µCi/kg) was administered IP to male offspring, 15 minutes before sacrifice. By liquid scintillation spectroscopy, ³H-activity (expressed as disintegrations per minute [DPM]) was determined in discrete parts of the brain and some peripheral tissues, and expressed as DPM/100 mg of tissue, wet weight. It was found that the highest amount of zinc was accumulated in the brain and liver of rat offspring that were exposed to zinc postnatally. [³H]-activity was at lower levels, in comparison, in nearly all other parts of the brain of rats exposed to zinc postnatally. In offspring receiving zinc prenatally, zinc levels were at similar or lower amounts in the brain and peripheral tissues, vs. the group with postnatal exposure. From this study in rats we conclude that zinc accumulates to the highest extent in brain, following a later ontogenetic (postnatal) exposure period, and by this, there is also greater disturbance of metabolic processes associated with glucose utilization.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.