In hypertension, the kidney is not always the heart of the matter.
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.
Mendelsohn
Michael E
ME
Molecular Cardiology Research Institute, Tufts-New England Medical Center, Boston, Massachusetts, USA.
D000818:Animals; D001808:Blood Vessels / Q000002:abnormalities* / Q000166:cytology / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000502:physiology*; D016030:Kidney Transplantation; D051379:Mice; D008822:Mice, Transgenic; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism
D044140:Receptor, Angiotensin, Type 1