Skip to main content

EDITORIAL article

Front. Med., 19 February 2020
Sec. Nephrology
This article is part of the Research Topic Renal Hypertension at the Crossroads: Theoretical, Experimental and Clinical Aspects View all 7 articles

Editorial: Renal Hypertension at the Crossroads: Theoretical, Experimental and Clinical Aspects

  • 1Nephrology/Intensive Care, Charité Medical University of Berlin, Berlin, Germany
  • 2Department of Internal Medicine and Geriatrics, University of Greifswald, Greifswald, Germany
  • 3Experimental and Clinical Research Center, Charite University Medicine Berlin, Berlin, Germany
  • 4Department of Internal Medicine and Nephrology, University Medicine Marburg, Marburg, Germany

Since Goldblatt's seminal experiment in Goldblatt et al. (1), renal hypertension has increasingly been recognized as an important cause of secondary hypertension and chronic kidney disease, the latter by virtue of renal ischemia. Followed later by important work, the scientific community recognized that renal artery occlusion does not only increase systemic blood pressure by decreased transstenotic blood flow but by an array of multiple systemic or local mechanisms, which all contribute to high blood pressure and hypertension-related injury. The contributions made in this Frontiers Research Topic are significant because they add to considerations that have been given to the kidney in hypertension and relative to its role in vascular function. The control of renal and cardiovascular hemodynamics and renal function in hypertension was elegantly discussed (Sata et al.). Resistant hypertension is generally defined as uncontrolled blood pressure (>140/90 mm Hg) after treatment with three or more antihypertensives. Salt sensitivity was studied in resistant hypertension and renal denervation using an in vitro erythrocyte salt sedimentation assay (Vonend et al.). Alamandine and its receptor were identified as novel protective contributors to the renin-angiotensin system (Schleifenbaum). A novel hierarchical statistical method and genetically encoded calcium indicators (GECIs) have been implemented in experimental hypertension (Tsvetkov et al.; Zhong and Schleifenbaum). Caveolae associated signal transduction pathways were identified in vasculature to play important pathophysiological role in hypertension (Lian et al.). Together, the authors explicitly place findings that can be taken advantage of in creating new therapies and experimental models for cardiovascular diseases that continue to challenge our community. These include resistant hypertension, renal artery interventions, therapeutic targeting of endothelial cells and perivascular adipose tissue, and salt consumption in health and disease to name a few. We are grateful to our contributors for sharing their important work.

Author Contributions

All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

The Deutsche Forschungsgemeinschaft (DFG) supported our work.

References

1. Goldblatt H, Lynch J, Hanzal RF, Summerville WW. Studies on experimental hypertension: I. The production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med. (1934) 59:347–79.

PubMed Abstract | Google Scholar

Keywords: hypertension, perivascular adipose tissue, renal denervation, caveolae, alamandine

Citation: Gollasch M and Hoyer J (2020) Editorial: Renal Hypertension at the Crossroads: Theoretical, Experimental and Clinical Aspects. Front. Med. 7:49. doi: 10.3389/fmed.2020.00049

Received: 23 October 2019; Accepted: 31 January 2020;
Published: 19 February 2020.

Edited and reviewed by: Robert P. Woroniecki, Stony Brook Children's Hospital, United States

Copyright © 2020 Gollasch and Hoyer. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Maik Gollasch, maik.gollasch@charite.de

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.