title: The kidney and hypertension:  novel insights from transgenic models.
abstract: OBJECTIVE
  Despite decades of study, the pathogenesis of essential hypertension remains obscure, but the kidney appears to play a central role. Technology for manipulation of the mouse genome has been immensely valuable in dissecting pathways involved in blood pressure control. This review summarizes recent studies employing this technology to understand signaling pathways and specific cell lineages within the kidney that are involved in the regulation of sodium excretion impacting blood pressure homeostasis.
  
  
  RESULTS
  We review a series of recent studies of regulatory pathways affecting sodium excretion by the kidney including the renin-angiotensin system, the mineralocorticoid receptor, the endothelin system, nitric oxide, and the with-no-lysine (K)/sterile 20-like kinase pathway. We have specifically highlighted studies utilizing transgenic mouse models, which provide a powerful mechanism for defining the role of proteins and pathways on sodium balance and blood pressure in the intact organism.
  
  
  CONCLUSIONS
  These studies underscore the importance of the kidney in regulation of blood pressure and the pathogenesis of hypertension. Transgenic mouse models provide a powerful approach to identifying key cell lineages and molecular pathways causing hypertension. These pathways represent potential targets for novel antihypertensive therapies.
authors.affiliation: Division of Nephrology, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.
authors.forename: Marcela
authors.initials: M
authors.lastname: Herrera
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Coffman
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001794:Blood Pressure; D004298:Dopamine / Q000096:biosynthesis; D019332:Endothelin-1 / Q000378:metabolism; D006973:Hypertension / Q000209:etiology*; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D051379:Mice / Q000235:genetics; D009318:Natriuresis; D009569:Nitric Oxide; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D018161:Receptors, Mineralocorticoid; D012084:Renin-Angiotensin System / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics*; D012964:Sodium / Q000378:metabolism
chemical_list: D019332:Endothelin-1; D044140:Receptor, Angiotensin, Type 1; D018161:Receptors, Mineralocorticoid; D009569:Nitric Oxide; D012964:Sodium; C486407:Stk39 protein, mouse; D017346:Protein Serine-Threonine Kinases; D004298:Dopamine