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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
Author(s) -
Berg T. N. A. Daniëlle,
Thijssen Dick H. J.,
Mil Anke C. C. M.,
Broek Petra H.,
Rongen Gerard A.,
Monajemi Houshang,
Deinum Jaap,
Riksen Niels P.
Publication year - 2019
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.13180
Subject(s) - medicine , adenosine , primary aldosteronism , endocrinology , adenosine receptor , brachial artery , blood pressure , cardiology , receptor , agonist
Abstract Background Patients with primary aldosteronism (PA) experience more cardiovascular events compared to patients with essential hypertension (EHT), independent from blood pressure levels. In animals, mineralocorticoid receptor antagonists limit ischaemia‐reperfusion (IR) injury by increasing extracellular adenosine formation and adenosine receptor stimulation. Adenosine is an endogenous compound with profound cardiovascular protective effects. Firstly, we hypothesized that patients with PA have lower circulating adenosine levels which might contribute to the observed increased cardiovascular risk. Secondly, we hypothesized that by this mechanism, patients with PA are more susceptible to IR compared to patients with EHT. Design In our prospective study in 20 patients with PA and 20 patients with EHT, circulating adenosine was measured using a pharmacological blocker solution that halts adenosine metabolism after blood drawing. Brachial artery flow‐mediated dilation (FMD) before and after forearm IR was used as a well‐established method to study IR injury. Results Patients with PA had a 33% lower adenosine level compared to patients with EHT (15.3 [13.3‐20.4] vs 22.7 [19.4‐36.8] nmol/L, respectively, P < .01). The reduction in FMD after IR, however, did not differ between patients with PA and patients with EHT (−1.0 ± 2.9% vs −1.6 ± 1.6%, respectively, P = .52). Conclusions As adenosine receptor stimulation induces various powerful protective cardiovascular effects, its lower concentration in patients with PA might be an important novel mechanism that contributes to their increased cardiovascular risk. We suggest that modulation of the adenosine metabolism is an exciting novel pharmacological opportunity to limit cardiovascular risk in patients with PA that needs further exploration.