Plasma levels of the cardiovascular protective endogenous nucleoside adenosine are reduced in patients with primary aldosteronism without affecting ischaemia‐reperfusion injury: A prospective case‐control study-Reference-Cited by-同舟云学术

Plasma levels of the cardiovascular protective endogenous nucleoside adenosine are reduced in patients with primary aldosteronism without affecting ischaemia‐reperfusion injury: A prospective case‐control study

Published:2019-11-25 Issue:12 Volume:49 Page:
ISSN:0014-2972
Container-title:European Journal of Clinical Investigation
language:en
Short-container-title:Eur J Clin Invest

Author:

Berg T. N. A. (Daniëlle)¹²^ORCID,Thijssen Dick H. J.³,Mil Anke C. C. M.³,Broek Petra H.¹,Rongen Gerard A.¹²,Monajemi Houshang⁴,Deinum Jaap²⁵,Riksen Niels P.²

Affiliation:

1. Department of Pharmacology‐Toxicology Radboud university medical center Nijmegen The Netherlands

2. Department of Internal Medicine Radboud university medical center Nijmegen The Netherlands

3. Department of Physiology Radboud university medical center Nijmegen The Netherlands

4. Department of Internal Medicine Rijnstate Ziekenhuis Arnhem The Netherlands

5. Department of Internal Medicine III University Hospital Carl Gustav Carus Technische Universität Dresden Dresden Germany

Publisher

Wiley

Subject

Clinical Biochemistry,Biochemistry,General Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/eci.13180

Reference56 articles.

1. PROGRESS IN ALDOSTERONISM: A review of the prevalence of primary aldosteronism in pre-hypertension and hypertension

2. Cardiovascular events and target organ damage in primary aldosteronism compared with essential hypertension: a systematic review and meta-analysis

3. Association of elevated plasma aldosterone-to-renin ratio with future cardiovascular events in patients with essential hypertension

4. The Effect of Spironolactone on Morbidity and Mortality in Patients with Severe Heart Failure

5. Eplerenone, a Selective Aldosterone Blocker, in Patients with Left Ventricular Dysfunction after Myocardial Infarction

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