Role of AT1 receptor-mediated salt retention in angiotensin II-dependent hypertension

Steven D. Crowley, Jiandong Zhang, Maria Herrera, Robert Griffiths, Phillip Ruiz, Thomas M. Coffman

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


Activation of type 1 angiotensin II (AT1) receptors in the kidney promotes blood pressure elevation and target organ damage, but whether renal AT1 receptors influence the level of hypertension by stimulating sodium retention or by raising systemic vascular resistance has not been established. In the current studies, we used a kidney cross-transplantation strategy to determine whether increased sodium reabsorption by AT1 receptors in the kidney mediates the chronic hypertensive response to angiotensin II. We found this to be true. In addition, we also identified a second, nontrivial component of blood pressure elevation induced by activation of renal AT1 receptors that is sodium-independent. As the kidney has the capacity to limit the transmission of elevated systemic blood pressure into the renal microcirculation, prior studies struggled to clearly discriminate the relative contributions of blood pressure elevation vs. activation of AT1 receptors to hypertensive kidney injury. In our model, we found that rapid surges in blood pressure, which may overcome the kidney's capacity to prevent perturbations in renal hemodynamics, correlate closely with kidney damage in hypertension. Moreover, maximal kidney injury in hypertension may require activation of a pool of nonrenal, systemic AT1 receptors. These studies provide insight into precise mechanisms through which AT1 receptor blockade influences the progression of hypertensive kidney disease.

Original languageEnglish (US)
Pages (from-to)F1124-F1130
JournalAmerican Journal of Physiology - Renal Physiology
Issue number5
StatePublished - Nov 2011


  • Kidney diseases

ASJC Scopus subject areas

  • Physiology
  • Urology
  • Medicine(all)


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