Ändra sökning
RefereraExporteraLänk till posten
Permanent länk

Direktlänk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Mechanisms by which intrarenal dopamine and ANP interact to regulate sodium metabolism
2000 (Engelska)Ingår i: Clinical and experimental hypertension (1993, Print), ISSN 1064-1963, E-ISSN 1525-6006, Vol. 22, nr 3, s. 303-307Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Maintenance of a normal blood pressure requires a precise and fine-tuned regulation of salt metabolism. This is accomplished by a bidirectional regulation of renal tubular sodium transporters by natriuretic and antinatriuretic hormones. Dopamine, produced in the renal proximal tubular cells, plays an important role in this interactive system. Dopamine inhibits the activity of Na+,K(+)ATPase as well as of many important sodium influx pathways in the nephron. These effects of dopamine are particularly pronounced in situation of sodium loading. There is an abundance of evidence suggesting that the natriuretic effects of ANP are to a large extent mediated via renal dopamine 1 like receptors. The renal tubular dopamine 1 like receptors are, under basal conditions, mainly located intracellularly. ANP and its second messenger, cGMP, cause a rapid translocation of the dopamine 1 like receptors to the plasma membrane. This phenomenon may explain how ANP and dopamine act in concert to regulate sodium metabolism Regulation of sodium metabolism and blood pressure is critically dependent on a normal function of the renal dopamine system. Hence, abnormalities in the interaction between dopamine and ANP may predispose to hypertension.

Ort, förlag, år, upplaga, sidor
2000. Vol. 22, nr 3, s. 303-307
Nyckelord [en]
dopamine receptors, Na+,K+ ATPase, DARPP-32, k+-atpase activity, atrial-natriuretic-factor, renal tubule cells, brush-border membrane, thick ascending limb, na+-h+ antiport, na+,k+-atpase activity, endogenous dopamine, rat, inhibition
Identifikatorer
URN: urn:nbn:se:kth:diva-19730ISI: 000086811300007OAI: oai:DiVA.org:kth-19730DiVA, id: diva2:338422
Anmärkning
QC 20100525Tillgänglig från: 2010-08-10 Skapad: 2010-08-10 Senast uppdaterad: 2017-12-12Bibliografiskt granskad

Open Access i DiVA

Fulltext saknas i DiVA

Personposter BETA

Brismar, Hjalmar

Sök vidare i DiVA

Av författaren/redaktören
Brismar, Hjalmar
I samma tidskrift
Clinical and experimental hypertension (1993, Print)

Sök vidare utanför DiVA

GoogleGoogle Scholar

urn-nbn

Altmetricpoäng

urn-nbn
Totalt: 45 träffar
RefereraExporteraLänk till posten
Permanent länk

Direktlänk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf