Journal
JCI INSIGHT
Volume 7, Issue 24, Pages -Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.161765
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Funding
- Common Fund of the Office of the Director of the NIH
- National Cancer Institute (NCI)
- National Human Genome Research Institute
- National Heart, Lung, and Blood Institute
- National Institute on Drug Abuse, National Institute of Mental Health
- National Institute of Neurological Disorders and Stroke
- NCI/NIH Cancer Center Support Grant [P30CA068485]
- NIH [DK51265, DK95785, DK62794, DK7569, P30DK114809, DK116964, DK069921, DK127589]
- VA Merit Award [00507969]
- VA Merit [I01-BX002196]
- ASN Kidney Cure career development award
- Intramural Research Program of the NIH
- National Institute of Environmental Health Sciences [ES103361-01]
- Vanderbilt Center for Kidney Disease, and Clinical and Translational Science Awards from the National Center for Advancing Translational Sciences [UL1 TR002243]
- NCl
- NCI NIH Cancer Center Support Grant [5P30 CA68485-19]
- American Heart Association
- American Society of Nephrology
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Research has found that vasopressin can be produced in the kidneys, specifically in the tubular epithelial cells of mouse and human kidneys. This kidney-derived vasopressin is biologically active and regulated by hypertonic conditions and water restriction.
Vasopressin has traditionally been thought to be produced by the neurohypophyseal system and then released into the circulation where it regulates water homeostasis. The questions of whether vasopressin could be produced outside of the brain and if the kidney could be a source of vasopressin are raised by the syndrome of inappropriate antidiuretic hormone secretion (vasopressin). We found that mouse and human kidneys expressed vasopressin mRNA. Using an antibody that detects preprovasopressin, we found that immunoreactive preprovasopressin protein was found in mouse and human kidneys. Moreover, we found that murine collecting duct cells made biologically active vasopressin, which increased in response to NaCl-mediated hypertonicity, and that water restriction increased the abundance of kidney-derived vasopressin mRNA and protein expression in mouse kidneys. Thus, we provide evidence of biologically active production of kidney -derived vasopressin in kidney tubular epithelial cells.
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