Endocrine Abstracts

Background: The renin-angiotensin-aldosterone system (RAS) constitutes a key hormonal system in the physiological and pathological regulation of blood pressure. In effort to understand complex and multifunctional aspects of this system, current biochemical approaches target to characterize and define its various components with angiotensin II being in the mainstream.

Objective: The aim of this study was to evaluate concentrations of angiotensin II in hypertensive patients undergoing laboratory screening for primary aldosteronism.

Methodology: Plasma aldosterone, angiotensin II and direct renin concentrations from 49 patients (including 11 with primary hyperaldosteronism, 22%) were analyzed. Patients were taking most of their antihypertensive drugs, excluding mineralocorticoid receptor blockers. Angiotensin II was measured by two distinct, thus available in our conditions, methods: immunoassay (ELISA without previous chromatographic separation) and LC-MS/MS.

Results: Median ELISA Angiotensin II concentrations in primary aldosteronism patients were lower than in the control group: 689 pg/ml (IQR: 444.49–897.3) vs 873.18 pg/ml (IQR: 689.99–1267.63). However, the difference was not statistically significant. Surprisingly, if measured by LC-MS/MS, Angiotensin II showed the opposite trend. Median LC-MS/MS Ang II was 475.34 pg/ml (IQR: 253.77–520.79) in primary aldosteronism patients compared to median 123.66 pg/ml (IQR: 72.15–251.87) in the control group (P=0.0248). If calculated as ratios with aldosterone, only ELISA angiotensin II concentrations showed statistical significance. Areas under the receiver operation characteristic curve (AUROC) for aldosterone-to-angiotensin II ratio (AA2R) and aldosterone-to-renin ratio (ARR) were 0.79 and 0.92 accordingly, despite ongoing antihypertensive therapy.

Conclusions: The accurate assessment of angiotensin peptides is the next step to ascertain the status of the RAS, particularly in pathological conditions or under the influence of interfering therapeutic agents. However, such evaluation is hampered by many factors. They contribute to the marked variability in angiotensin values evident in the literature and raise concerns on the identity of angiotensin II detected in the circulation. Therefore, the question if the extent to that altered peptide content truly reflects or contributes to a particular phenotype, still requires more studies and, most of all, ubiquitous technical progress.