In hypertension, the kidney is not always the heart of the matter

J Clin Invest. 2005 Apr;115(4):840-4. doi: 10.1172/JCI24806.

Abstract

Blood pressure abnormalities are thought to originate from intrinsic changes in the kidney, a concept that has been largely unchallenged for more than 4 decades. However, recent molecular, cellular, and transgenic mouse studies support an alternative hypothesis: primary abnormalities in vascular cell function can also directly cause abnormalities of blood pressure. In this issue of the JCI, Crowley and coworkers describe the application of an elegant cross-renal transplant model to type 1A angiotensin (AT(1A)) receptor-deficient mice and their wild-type littermates to explore the relative contributions of renal and extrarenal tissues to the low blood pressure seen in the AT(1A) receptor-deficient animals. Their studies further support the emerging paradigm that primary abnormalities of the vasculature can make unique, nonredundant contributions to blood pressure regulation; the findings have potentially important implications for the ways we diagnose and treat blood pressure diseases in humans.

Publication types

  • Comment

MeSH terms

  • Animals
  • Blood Vessels / abnormalities*
  • Blood Vessels / cytology
  • Blood Vessels / metabolism
  • Humans
  • Hypertension / physiopathology*
  • Kidney / physiology*
  • Kidney Transplantation
  • Mice
  • Mice, Transgenic
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / metabolism
  • Myocytes, Smooth Muscle / metabolism
  • Receptor, Angiotensin, Type 1 / genetics
  • Receptor, Angiotensin, Type 1 / metabolism

Substances

  • Receptor, Angiotensin, Type 1