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10.4414/smw.2012.13613

http://scihub22266oqcxt.onion/10.4414/smw.2012.13613
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22802123!ä!22802123

suck abstract from ncbi


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pmid22802123      Swiss+Med+Wkly 2012 ; 142 (ä): w13613
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  • Physiopathology of hereditary polyuric states: a molecular view of renal function #MMPMID22802123
  • Bichet DG
  • Swiss Med Wkly 2012[]; 142 (ä): w13613 PMID22802123show ga
  • Recent discoveries have shed new light on the understanding of water metabolism: (1.) in addition to hypothalamic osmoreceptor cells expressing a TRPV1 variant, there are peripheral TRPV4 receptors sensing tonicity in the portal vein and changing central vasopressin secretion and peripheral autonomic activity; (2.) the central osmoregulatory gain of angiotensin action participates in the non-osmotic release of vasopressin induced by hypovolaemia; (3.) prostaglandins EP2 receptors on principal cells of the collecting ducts positively regulate urine concentration mechanisms. These new developments are important clinically for the understanding of hereditary polyuric states. We recommend sequencing of the nephrogenic diabetes insipidus genes in all affected patients. This genomic information is key to the routine care of patients with congenital polyuria and, as in other genetic diseases, reduces health costs and confers psychological benefits on patients and families.
  • |Arginine Vasopressin/biosynthesis/physiology[MESH]
  • |Diabetes Insipidus/*genetics/physiopathology[MESH]
  • |Humans[MESH]
  • |Kidney/*physiopathology[MESH]
  • |Neurons, Afferent/metabolism[MESH]
  • |Osmolar Concentration[MESH]
  • |Polyuria/genetics/*physiopathology[MESH]
  • |Sodium/blood[MESH]
  • |TRPV Cation Channels/metabolism[MESH]


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