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Renal dopamine receptors and hypertension.

Abstract
Dopamine has been recognized as an important modulator of central as well as peripheral physiologic functions in both humans and animals. Dopamine receptors have been identified in a number of organs and tissues, which include several regions within the central nervous system, sympathetic ganglia and postganglionic nerve terminals, various vascular beds, the heart, the gastrointestinal tract, and the kidney. The peripheral dopamine receptors influence cardiovascular and renal function by decreasing afterload and vascular resistance and promoting sodium excretion. Within the kidney, dopamine receptors are present along the nephron, with highest density on proximal tubule epithelial cells. It has been reported that there is a defective dopamine receptor, especially D(1) receptor function, in the proximal tubule of various animal models of hypertension as well as in humans with essential hypertension. Recent reports have revealed the site of and the molecular mechanisms responsible for the defect in D(1) receptors in hypertension. Moreover, recent studies have also demonstrated that the disruption of various dopamine receptor subtypes and their function produces hypertension in rodents. In this review, we present evidence that dopamine and dopamine receptors play an important role in regulating renal sodium excretion and that defective renal dopamine production and/or dopamine receptor function may contribute to the development of various forms of hypertension.
AuthorsTahir Hussain, Mustafa F Lokhandwala
JournalExperimental biology and medicine (Maywood, N.J.) (Exp Biol Med (Maywood)) Vol. 228 Issue 2 Pg. 134-42 (Feb 2003) ISSN: 1535-3702 [Print] England
PMID12563019 (Publication Type: Journal Article, Review)
Chemical References
  • Receptors, Dopamine
  • Sodium
  • Protein-Tyrosine Kinases
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C
  • Phospholipases A
  • Type C Phospholipases
  • GTP-Binding Proteins
  • Adenylyl Cyclases
  • Dopamine
Topics
  • Adenylyl Cyclases (metabolism)
  • Animals
  • Cyclic AMP-Dependent Protein Kinases (metabolism)
  • Disease Models, Animal
  • Dopamine (metabolism)
  • Epithelial Cells (cytology, metabolism)
  • GTP-Binding Proteins (metabolism)
  • Humans
  • Hypertension (metabolism)
  • Kidney Tubules (cytology, metabolism)
  • Phospholipases A (metabolism)
  • Protein Kinase C (metabolism)
  • Protein-Tyrosine Kinases (metabolism)
  • Receptors, Dopamine (genetics, metabolism)
  • Second Messenger Systems (physiology)
  • Sodium (metabolism)
  • Type C Phospholipases (metabolism)

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