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Reply Correspondence discuss the putative pitfalls of a Guytonian interpretation of salt sensitivity of blood pressure, including the lack of a b differences in sodium balance, plasma volume and cardiac Theodore W. Kurtz , Stephen E. DiCarlo , c d output between salt-sensitive and salt-resistant individuals Michal Pravenec , and R. Curtis Morris Jr given a salt load. We have also published on this [6]. We would, therefore, suggest if these authors continue their crusade against ‘Guytonian dogma’ that they comment on e thank Drs Laffer and Elijovich for their interest new and important evidence. This includes the fact that salt [1] in our publication [2] focusing on the Amer- sensitivity can be experimentally produced by manipulat- W ican Heart Association (AHA) Scientific State- ing genes that are exclusively expressed in the kidney, ment on salt sensitivity [3]. To our knowledge, our without expression or known function in the vasculature, publication is the first to criticize the AHA Statement [3] such as uromodulin [7], and also by specific renal proximal as it pertains to the pathogenesis of salt sensitivity. We tubular knockout of other genes, which remain normally highlighted the point that all of the putative abnormalities expressed systemically, such http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Hypertension Wolters Kluwer Health

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Publisher
Wolters Kluwer
Copyright
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
ISSN
0263-6352
eISSN
1473-5598
D.O.I.
10.1097/HJH.0000000000001637
Publisher site
See Article on Publisher Site

Abstract

Correspondence discuss the putative pitfalls of a Guytonian interpretation of salt sensitivity of blood pressure, including the lack of a b differences in sodium balance, plasma volume and cardiac Theodore W. Kurtz , Stephen E. DiCarlo , c d output between salt-sensitive and salt-resistant individuals Michal Pravenec , and R. Curtis Morris Jr given a salt load. We have also published on this [6]. We would, therefore, suggest if these authors continue their crusade against ‘Guytonian dogma’ that they comment on e thank Drs Laffer and Elijovich for their interest new and important evidence. This includes the fact that salt [1] in our publication [2] focusing on the Amer- sensitivity can be experimentally produced by manipulat- W ican Heart Association (AHA) Scientific State- ing genes that are exclusively expressed in the kidney, ment on salt sensitivity [3]. To our knowledge, our without expression or known function in the vasculature, publication is the first to criticize the AHA Statement [3] such as uromodulin [7], and also by specific renal proximal as it pertains to the pathogenesis of salt sensitivity. We tubular knockout of other genes, which remain normally highlighted the point that all of the putative abnormalities expressed systemically, such

Journal

Journal of HypertensionWolters Kluwer Health

Published: Mar 1, 2018

References

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