INT390
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
(I.O.D.) of the hybridized dots revealed a 1-fold and 8-fold increase in Ang mNRA in rats receiving morphine injection for 1 and 4 days, respectively, and a 5-fold and 13-fold increase in rats receiving 3 and 6h EA stimulation, respectively. | |||||||||||||||
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Autoradiographic examination revealed a marked increase in Ang mRNA in rats receiving multiple injections of morphine or continuous electroacupuncture (EA) stimulation for several hours. | |||||||||||||||
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Using microbore high-performance liquid chromatography, we determined the concentrations of adenosine in plasma samples collected from (a) the left ventricle and jugular vein of anesthetized rats during acute intravenous infusions of angiotensin II (1, 10, and 100 ng/min) and (b) the carotid artery of conscious, unrestrained rats exposed to chronic elevations of either exogenous angiotensin II (intraperitoneal infusion of angiotensin II, 125 ng/min) or endogenous angiotensin II (induction of renovascular hypertension by clipping the left renal artery or by ligating the suprarenal aorta). | |||||||||||||||
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Using microbore high-performance liquid chromatography, we determined the concentrations of adenosine in plasma samples collected from (a) the left ventricle and jugular vein of anesthetized rats during acute intravenous infusions of angiotensin II (1, 10, and 100 ng/min) and (b) the carotid artery of conscious, unrestrained rats exposed to chronic elevations of either exogenous angiotensin II (intraperitoneal infusion of angiotensin II, 125 ng/min) or endogenous angiotensin II (induction of renovascular hypertension by clipping the left renal artery or by ligating the suprarenal aorta). | |||||||||||||||
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During enalaprilat infusion, interstitial fluid concentration of Ang I was significantly increased from 0.78+/-0.06 to 0.97+/-0.08 nmol/L; however, Ang II concentrations were not altered significantly (3.67+/-0.28 versus 3.67+/-0.25 nmol/L). | |||||||||||||||
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The present results show it to be a competitive antagonist also in vivo since pA2 values are similar, always reaches a 100% response on increasing the Angiotensin II dose, and when relating log (DR-1) and log dose of agonist, the slope is very near to one (0.925). | |||||||||||||||
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Experimental study in 156 white rats with renovascular hypertension, posthemorrhagic hypotension and with normal blood pressure revealed that high--ressure oxygen (303.9 kPa--50 min) could activate angiotensin--converting enzyme, the latter taking part in inactivation of endogenous opioid peptides. | |||||||||||||||
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Angiotensin II receptors are upregulated by estradiol and progesterone in the locus coeruleus, median preoptic nucleus and subfornical organ of ovariectomized rats. | |||||||||||||||
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In conclusion, these results show that Ang II receptors are upregulated by E(2) and P in the LC, MnPO and SFO of ovariectomized rats. | |||||||||||||||
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The main features of Bartter's syndrome are growth retardation, hypertrophy, and hyperplasia of the juxtaglomerular apparatus, increased angiotensin II, hyperaldosteronism, hypokalemic alkalosis, normal blood pressure, and decreased response to pressors. | |||||||||||||||
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Increased blood pressure and dipsogenic sensitivity to administration of angiotensin II (Ang II) have been demonstrated during the first 3 weeks of exposure to cold suggesting an upregulation of Ang II receptors when PRA is elevated. | |||||||||||||||
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Presumably, this can increase the amount of Ang II locally produced in the carotid body, which in turn causes an elevated level of Ang IV for the activation of intracellular signaling cascade leading to the [Ca2+]i elevation. | |||||||||||||||
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Hence, hypoxia induces an upregulation of the expression of AT4 receptors in the glomus cells of the carotid body with an increase in the Ang IV-induced [Ca2+]i elevation. | |||||||||||||||
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The effect of leucine5-enkephalin (Leu-enkephalin) administered into the lateral (LV) or fourth (4V) cerebroventricle on angiotensin II (ANG II)-stimulated increase in blood pressure, plasma vasopressin concentration ([AVP]), and drinking behavior was determined in conscious rats. | |||||||||||||||
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The effect of leucine5-enkephalin (Leu-enkephalin) administered into the lateral (LV) or fourth (4V) cerebroventricle on angiotensin II (ANG II)-stimulated increase in blood pressure, plasma vasopressin concentration ([AVP]), and drinking behavior was determined in conscious rats. | |||||||||||||||
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The effect of intracerebroventricular (i.c.v.) administration of leumorphin on basal blood pressure and angiotensin II (AII)-stimulated increase in blood pressure was examined in conscious unrestrained rats. | |||||||||||||||
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L-NAME or 7-nitroindazole enhanced the angiotensin II pressor effect (P < 0.05). | |||||||||||||||
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Enalaprilat resulted in a significant increase in plasma Ang I from 133+/-21 to 1167+/-328 pmol/L and a decrease in plasma Ang II from 110+/-12 to 67+/-9 pmol/L. | |||||||||||||||
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As previously seen with 5-HT agonists, the efficacy of PAT for displacing [3H]5-HT bound to hippocampal membranes was markedly increased by Mn2+ (1 mM) and reduced by GTP (0.1 mM). | |||||||||||||||
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In suckling rats, indomethacin suppressed PGE(2) and COX-2 expression, and increased PGF(2alpha), whereas ibuprofen increased COX-2 and angiotensin II. | |||||||||||||||
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General Comments
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