doi: 10.1161/01.RES.0000147313.80351.92
© 2004 American Heart Association, Inc.
Editorials |
Blood Pressure Control Goes Nuclear
From the Carolina Cardiovascular Biology Center and Departments of Medicine, Pharmacology, and Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC.
Correspondence to Cam Patterson, MD, Director, Carolina Cardiovascular Biology Center, University of North Carolina at Chapel Hill, 8200 Medical Biomolecular Research Building, Chapel Hill, NC 27599-7126. E-mail cpatters@med.unc.edu
See related article, pages 902–910
Key Words: endothelium • DNA repair • hypertension • nitric oxide
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The control of blood pressure is regulated with extreme precision, and requires integration of information from the central nervous system, the kidneys, the vasculature, and the heart. Salt and water balances, sympathetic activity, arterial stiffness, and the tone of resistance vessels determine the chronic regulation of intravascular pressure. It is a standard experiment for physicians-in-training to manipulate these activities using classical physiological techniques and observe the homeostatic mechanisms that return blood pressure to its normal levels. Given the many controls that exist to maintain blood pressure within a narrow and appropriate range, it is all the more remarkable that clinical hypertension is as common as it is, affecting more than 50 million Americans and 75% of the population older than 65 years of age.
The paracrine and endocrine mechanisms that regulate blood pressure are now reasonably well understood, and indeed provide the pharmacological basis for most antihypertensive therapies. In contrast, the intracellular events that tune blood pressure are less well characterized. In particular, nuclear events that control blood pressure are not well known. This is a major gap in our understanding of the problem insofar as long-term changes in gene regulation are a likely proximate cause of the systematic events that result in chronic hypertension. A report in this issue of Circulation Research by Irani and colleagues,1 which clearly defines a role for the multifunctional nuclear protein apurinic/apyrimidinic endonuclease (APE1, also known as redox factor-1) in chronic regulation of vascular tone in vivo, represents an important step toward understanding how
Related Article:
Circ. Res. 2004 95: 902-910.