INT84599
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
(b) Immunoblotting studies for AQP2 protein expression in the IMCD from injected rats and in IMCD tubules suspension from 10 normal rats incubated with 10(-7) M fluoxetine. (2) In vitro microperfusion study: The osmotic water permeability (P(f), mum/s) was determined in normal rats IMCD (n = 6), isolated and perfused by the standard methods. | |||||||||||||||
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This investigation focused on the possibility that this increase in free water clearance following administration of an alpha(2)-adrenoceptor agonist was associated with a reduction in medullary AQP-2 expression. | |||||||||||||||
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Regulation of aquaporin-2 expression by the alpha(2)-adrenoceptor agonist clonidine in the rat. | |||||||||||||||
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Interestingly, however, taurine supplementation does not significantly affect plasma AVP, urine osmolality [18] or renal aquaporin2 expression. | |||||||||||||||
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Additional groups of control, TD and TT rats (n=3/group), which were not subjected to ischemic injury, were used for determination of the potential impact of body taurine status on (baseline) renal AQP2 expression [22]. | |||||||||||||||
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In support of this notion, we now show that the increased baseline urine osmolality is indeed associated with an increase in the renal expression of AQP2, a process that is regulated by arginine vasopressin (AVP) and contributes to the increase in water permeability of the collecting ducts [24]. | |||||||||||||||
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The decreased AQP2 expression in CRF rats was not altered in response to candesartan treatment; 3) Candesartan treatment was associated with decreased NHE3 and TSC expression in CRF, which could be due to the Ang II AT1 receptor blockade and/or decreased aldosterone levels; and 4) BSC-1 expression was increased in both CRF groups and the increased expression of BSC-1 was more prominent in candesartan-treated CRF rats compared with vehicle-treated CRF rats. | |||||||||||||||
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Kidney expression of AQP2 was decreased in CRF rats, both vehicle-treated (CRF-V) and candesartan-treated (CRF-C) | |||||||||||||||
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Thus, these studies all provide firm evidence for the decreased of vasopressin-regulated water channel AQP2 expression and the significant defects in the collecting duct of the kidneys from CRF. | |||||||||||||||
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Semi-quantitative immunoblotting of whole kidney protein samples from CRF rats (remnant kidney) and sham-operated rats (corresponding right whole kidney) demonstrated that CRF rats, both vehicle-treated (57±9% of sham-operated control level, p<0.05) and candesartan-treated (54±6% of sham-operated control level, p<0.05), had significantly decreased AQP2 expression compared with sham-operated controls (Fig. 3, Table 2). | |||||||||||||||
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In the present study, we further examine whether Ang II AT1 receptor blocker candesartan treatment in rats with CRF, where plasma vasopressin and AngII levels are elevated, could alter the downregulation of renal AQP2 expression and decreased urine concentration which were already seen in CRF rats (7). | |||||||||||||||
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In contrast, the whole kidney AQP2 expression in CRF rats was not altered in response to candesartan treatment (Fig. 3, Table 2).
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In the present study, we aimed to examine the effects of AngII AT1 receptor blockade on the expression of major renal sodium transporters (NHE3, BSC-1, and TSC) and vasopressin-regulated aquaporin-2 (AQP2) in rats with an early stage of CRF induced by 5/6 nephrectomy. | |||||||||||||||
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In the present study, we aimed to examine the effects of AngII AT1 receptor blockade on the expression of major renal sodium transporters (NHE3, BSC-1, and TSC) and vasopressin-regulated aquaporin-2 (AQP2) in rats with an early stage of CRF induced by 5/6 nephrectomy. | |||||||||||||||
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Because renal prostaglandins are derived largely from cyclooxygenase-2 (COX-2), we hypothesized that treatment of NDI with a COX-2 inhibitor may relieve polyuria through increased expression of Na-K-2Cl cotransporter type 2 (NKCC2) in the thick ascending limb and aquaporin-2 (AQP2) in the collecting duct. | |||||||||||||||
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Because renal prostaglandins are derived largely from cyclooxygenase-2 (COX-2), we hypothesized that treatment of NDI with a COX-2 inhibitor may relieve polyuria through increased expression of Na-K-2Cl cotransporter type 2 (NKCC2) in the thick ascending limb and aquaporin-2 (AQP2) in the collecting duct. | |||||||||||||||
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As shown in Figure 3, taurine-deficient kidneys showed significantly higher levels of non-glycosylated (25 kD) and glycosylated (30-37 kD) forms of AQP 2 than the control and taurine treated groups, which both showed similar AQP 2 levels. | |||||||||||||||
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As shown in Figure 7, renal tubules of TT/IR group displaying cystic dilatations exhibited immunostaining for AQP1 (panel A) but not AQP2 (panel B). | |||||||||||||||
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In contrast, the present study examined on CRF rats did not show any difference in total kidney AQP2 expression and urine concentration between the NaCl-restricted CRF rats treated with candesartan and NaCl-retricted CRF rats treated with vehicle alone. | |||||||||||||||
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Next, we aimed to examine the changes of iNOS expression and activated macrophage infiltration in the kidney and the effects of iNOS inhibition on AQP2 and NKCC2 expression in LPS rats. | |||||||||||||||
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