INT149238

Context Info Confidence 0.66 First Reported 2005 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 5 Total Number 5 Disease Relevance 3.07 Pain Relevance 0.73

aging (Aqp2) plasma membrane (Aqp2) protein complex (Aqp2) transmembrane transport (Aqp2) lysosome (Aqp2) cytoplasm (Aqp2)

Anatomy Link Frequency duct 6 urine 2 Aqp2 (Rattus norvegicus)

Pain Link Frequency Relevance Heat COX-2 inhibitor 10 99.40 antagonist 7 96.90 cINOD 7 86.96 medulla 1 56.24 ischemia 11 50.00 Bioavailability 1 6.52 Inflammation 11 5.00 anesthesia 4 5.00 isoflurane 4 5.00 withdrawal 3 5.00

Disease Link Frequency Relevance Heat Polyuria 9 99.82 Diabetes Insipidus 17 98.94 Adrenal Insufficiency 2 91.64 Thyroid Disease 1 90.60 Pressure And Volume Under Development 8 89.96 Cirrhosis 2 89.12 Myocardial Infarction 3 88.44 Disease 7 86.96 INFLAMMATION 16 86.40 Acute Renal Failure 4 85.52

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Speculation

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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].

Positive_regulation (increase) of Gene_expression (expression) of AQP2 in ducts

1) Confidence 0.66 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2994366 Disease Relevance 0.09 Pain Relevance 0

Treatment with a vasopressin receptor antagonist reversed the consequence of non-osmotic increase in vasopressin release in these conditions and improved urinary dilution, and animal studies showed that AQP2 expression was increased [4,6].

Positive_regulation (increased) of Gene_expression (expression) of AQP2 associated with antagonist

2) Confidence 0.50 Published 2010 Journal BMC Nephrol Section Body Doc Link PMC2965705 Disease Relevance 0.78 Pain Relevance 0.05

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.

Positive_regulation (increased) of Gene_expression (expression) of aquaporin-2 in duct associated with polyuria, diabetes insipidus and cox-2 inhibitor

3) Confidence 0.49 Published 2008 Journal Am. J. Physiol. Renal Physiol. Section Abstract Doc Link 18216147 Disease Relevance 0.76 Pain Relevance 0.33

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.

Positive_regulation (increased) of Gene_expression (expression) of AQP2 in duct associated with polyuria, diabetes insipidus and cox-2 inhibitor

4) Confidence 0.49 Published 2008 Journal Am. J. Physiol. Renal Physiol. Section Abstract Doc Link 18216147 Disease Relevance 0.76 Pain Relevance 0.33

Interestingly, in a parallel study, we found that treatment with the AT1 receptor blocker candesartan in NaCl-restricted normal rats prevented the increase of the expression of inner medullary AQP2 and phosphorylated-AQP2 (AQP2 phosphorylated in the PKA-phosphorylation consensus site Ser-256) and the increase of urine concentration in response to the long-term dDAVP treatment (25).

Positive_regulation (increase) of Gene_expression (expression) of AQP2 in urine

5) Confidence 0.38 Published 2005 Journal Journal of Korean Medical Science Section Body Doc Link PMC2808601 Disease Relevance 0.68 Pain Relevance 0.03

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