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Oriji GK 《Prostaglandins, leukotrienes, and essential fatty acids》2003,68(3):233-238
Chronic treatment with cyclosporine A (CsA), a potent immunosuppressive agent, is associated with the development of arterial hypertension. The effect of CsA on vascular responses was determined in Sprague-Dawley rats and rat aortic rings. Male rats weighing 250-300 g were given either CsA (25mg/kg/day) in olive oil or vehicle by intraperitoneal (ip) injection for 7 days. CsA administration produced a 42% increase (P<0.001) in mean arterial pressure (MAP) which reached a plateau after 3 days. The level of both nitrate/nitrite (NO(2)/NO(3)), metabolites of nitric oxide (NO), decreased by 50% (P<0.001), but the level of thromboxane A2 (TBXA2) increased by 75% (P<0.001), in the urine. When 10(-9)M of CsA was added acutely to intact aortic rings from untreated rats, NO(2)/NO(3) production decreased by 83% (P<0.011), but TBXA2 production increased by 86% (P<0.001). The effects of CsA were reversed both in vivo and in vitro by pretreatment with metoprolol (15 mg/kg/day ip), B1-adrenoceptor antagonist. There were no changes in MAP and tension in rats treated with metoprolol alone. In addition, in aorta of rats that were treated with CsA ip for 7 days, CsA significantly activated protein kinase C (PKC) translocation. This suggests that PKC mediate, in part, CsA-induced hypertension. In summary, CsA inhibits endothelial NO formation, activate PKC, and increase TBXA2 production, with resulting increase in MAP, and this changes can be overcome by pretreatment with metoprolol. 相似文献
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G K Oriji 《Prostaglandins, leukotrienes, and essential fatty acids》1999,61(1):41-44
Cyclosporine A (CsA) is an immunosuppressive agent, which also causes hypertension. The effect of CsA on vascular responses was determined in spontaneously hypertensive rats and isolated rat aortic rings. Male rats weighing 250-300 g were given either CsA (25 mg/kg/day) in olive oil or vehicle by i.p. injection for 7 days. CsA administration produced a 27% increase (P < 0.001) in mean arterial pressure (MAP) which reached a plateau after 3 days. Conversely, the level of nitrate/nitrite, metabolites of nitric oxide (NO), decreased by 44% (P < 0.001) in the urine. In the presence of endothelin (ET) 10(-9) M, thoracic aortic rings from rats treated with olive oil, L-Arginine (L-Arg) or L-Arg+CsA showed a 100% increase (P < 0.001) in tension compared to the aortic rings from rats treated with CsA alone; aortic rings from rats treated with CsA alone did not respond to ET. The effects of CsA were reversed in both in vivo and in vitro by pretreatment with L-Arg (10 mg/kg/day ip), the precursor of NO. There were no changes in MAP and tension in rats treated with L-Arg alone. Possible explanation for lack of response to ET of aortic rings from CsA treated rats may be that CsA affected ET signalling pathway; ET receptors mRNA (messenger ribonucleic acid) gene expression was inhibited in aortic rings of rats treated with CsA. In summary, CsA inhibits endothelial NO formation, with resulting increases in MAP, and this inhibition can be overcome by parenteral administration of L-Arg. 相似文献
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The evolutionary origin of the pinnipeds (seals, sea lions, and walruses)
is still uncertain. Most authors support a hypothesis of a monophyletic
origin of the pinnipeds from a caniform carnivore. A minority view suggests
a diphyletic origin with true seals being related to the mustelids (otters
and ferrets). The phylogenetic relationships of the walrus to other
pinniped and carnivore families are also still particularly problematic.
Here we examined the relative support for mono- and diphyletic hypotheses
using DNA sequence data from the mitochondrial small subunit (12S) rRNA and
cytochrome b genes. We first analyzed a small group of taxa representing
the three pinniped families (Phocidae, Otariidae, and Odobenidae) and
caniform carnivore families thought to be related to them. We inferred
phylogenetic reconstructions from DNA sequence data using standard
parsimony and neighbor-joining algorithms for phylogenetic inference as
well as a new method called spectral analysis (Hendy and Penny) in which
phylogenetic information is displayed independently of any selected tree.
We identified and compensated for potential sources of error known to lead
to selection of incorrect phylogenetic trees. These include sampling error,
unequal evolutionary rates on lineages, unequal nucleotide composition
among lineages, unequal rates of change at different sites, and
inappropriate tree selection criteria. To correct for these errors, we
performed additional transformations of the observed substitution patterns
in the sequence data, applied more stringent structural constraints to the
analyses, and included several additional taxa to help resolve long,
unbranched lineages in the tree. We find that there is strong support for a
monophyletic origin of the pinnipeds from within the caniform carnivores,
close to the bear/raccoon/panda radiation. Evidence for a diphyletic origin
was very weak and can be partially attributed to unequal nucleotide
compositions among the taxa analyzed. Subsequently, there is slightly more
evidence for grouping the walrus with the eared seals versus the true
seals. A more conservative interpretation, however, is that the walrus is
an early, but not the first, independent divergence from the common
pinniped ancestor.
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G K Oriji 《Prostaglandins, leukotrienes, and essential fatty acids》1999,61(2):119-123
Chronic treatment with the immunosuppressive drug Cyclosporine A (CsA) is associated with increased intracellular calcium in vascular smooth muscle cells, which may activate phospholipase A2. We used rat aortic endothelial cells to investigate the role of protein kinase C (PKC) in CsA-induced prostacyclin (PGI2) release. CsA (10(-9) M) produced a significant increase in PGI2 release. CsA-induced PGI2 release were inhibited 80-85% by 10(-9) M, and 99-100% by 10(-6) M pretreatment doses of any of three different PKC inhibitors, i.e. 1-(5-isoquinolinesulfonylmethyl)piperazine(H7), staurosporine or 1-(5-isoquinolinesulfonyl)piperazine. Pretreatment with (10(-9) M) of diltiazem (a voltage-sensitive L-type calcium channel blocker) completely inhibited both CsA-induced PGI2 release. Conversely, pretreatment with (10(-9) M) of thapsigargin (an intracellular calcium channel blocker) did not alter the action of CsA. These results strongly suggest that PKC, in association with an influx of extracellular calcium, mediates CsA-induced PGI2 release in rat aortic endothelial cells. 相似文献
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John Oriji 《Dialectical Anthropology》2007,31(1-3):263-288
This study examines the politico-religious structure of Igbo mini states and the diverse factors that led to the end of sacred authority and the moral codes of governance in the mini states since the pre-colonial period. The study provides some insights into the consequences of the desacralization of authority, and offers some suggestions that may be helpful in the preservation of ancient Igbo political institutions and the moral values associated with them. 相似文献
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Cyclosporine A (CsA) is an immunosuppressive agent, which also causes hypertension. The effect of CsA on vascular responses was determined in Sprague-Dawley rats and rat aortic rings. Male rats weighing 250-300 g were given either CsA (25 mg/kg/day) in olive oil or vehicle by intraperitoneal (ip) injection for 7 days. CsA administration produced a 42% increase (P < 0.001) in mean arterial pressure (MAP) which reached a plateau after 3 days. The level of both nitrate/nitrite (NO2/NO3), metabolites of nitric oxide (NO), decreased by 50% (P < 0.001), but the level of thromboxane A2 (TBXA2) increased by 75% (P < 0.001), in the urine. When 10(-9) M of CsAwas added acutely to intact aortic rings from untreated rats, NO2/NO3 production decreased by 83% (P < 0.011), but TBXA2 production increased by 86% (P < 0.001). The effects of CsA were reversed both in vivo and in vitro by pretreatment with propranolol (15 mg/kg/day ip), beta-adrenoceptor antagonist. There were no changes in MAP and tension in rats treated with prop alone. In addition, in aorta of rats that were treated with CsA ip for 7 days, CsA significantly activated protein kinase C (PKC) translocation. This suggests that PKC mediate, in part, CsA-induced hypertension. In summary, CsA inhibits endothelial NO formation, activate PKC, and increaseTBXA2 production, with resulting increase in MAP, and this changes can be overcome by pretreatment with propranolol. 相似文献