Influence of Antihypertensive Treatment on RAAS Peptides in Newly Diagnosed Hypertensive Patients
Annina S. Vischer,
Gabriela M. Kuster,
Raphael Twerenbold,
Otmar Pfister,
Qian Zhou,
Andrea Villiger,
Marko Poglitsch,
Stephan Krähenbühl,
Michael Mayr,
Stefan Osswald,
Manuel Haschke,
Thilo Burkard
Affiliations
Annina S. Vischer
Hypertension Clinic, Medical Outpatient Department and Hypertension Clinic, ESH Hypertension Centre of Excellence, University Hospital Basel, 4031 Basel, Switzerland
Gabriela M. Kuster
Clinic of Cardiology, University Hospital Basel, 4031 Basel, Switzerland
Raphael Twerenbold
Clinic of Cardiology, University Hospital Basel, 4031 Basel, Switzerland
Otmar Pfister
Clinic of Cardiology, University Hospital Basel, 4031 Basel, Switzerland
Qian Zhou
Clinic of Cardiology, University Hospital Basel, 4031 Basel, Switzerland
Andrea Villiger
Division of Clinical Pharmacology & Toxicology, University Hospital Basel, 4031 Basel, Switzerland
Marko Poglitsch
Attoquant Diagnostics GmbH, 1110 Vienna, Austria
Stephan Krähenbühl
Division of Clinical Pharmacology & Toxicology, University Hospital Basel, 4031 Basel, Switzerland
Michael Mayr
Hypertension Clinic, Medical Outpatient Department and Hypertension Clinic, ESH Hypertension Centre of Excellence, University Hospital Basel, 4031 Basel, Switzerland
Stefan Osswald
Clinic of Cardiology, University Hospital Basel, 4031 Basel, Switzerland
Manuel Haschke
Division of Clinical Pharmacology & Toxicology, University Hospital Basel, 4031 Basel, Switzerland
Thilo Burkard
Hypertension Clinic, Medical Outpatient Department and Hypertension Clinic, ESH Hypertension Centre of Excellence, University Hospital Basel, 4031 Basel, Switzerland
(1) Background: Recently, influences of antihypertensive treatment on the renin–angiotensin–aldosterone system (RAAS) has gained attention, regarding a possible influence on inflammatory and anti-inflammatory pathways. We aimed to study the effects of newly initiated antihypertensive drugs on angiotensin (Ang) II and Ang (1–7) as representers of two counter-regulatory axes. (2) Methods: In this randomized, open-label trial investigating RAAS peptides after the initiation of perindopril, olmesartan, amlodipine, or hydrochlorothiazide, Ang II and Ang (1–7) equilibrium concentrations were measured at 8 a.m. and 12 a.m. at baseline and after four weeks of treatment. Eighty patients were randomized (1:1:1:1 fashion). (3) Results: Between the four substances, we found significant differences regarding the concentrations of Ang II (p p = 0.019 for 8 a.m., p = 0.002), and increased by olmesartan (p p = 0.012), and hydrochlorothiazide (p = 0.001). Ang (1–7) was increased by perindopril and olmesartan (p = 0.008/0.002), but not measurably altered by amlodipine and hydrochlorothiazide (p = 0.317/ 0.109). (4) Conclusion: The initiation of all first line antihypertensive treatments causes early and distinct alterations of equilibrium angiotensin levels. Given the additional AT1R blocking action of olmesartan, RAAS peptides shift upon initiation of perindopril and olmesartan appear to work in favor of the anti-inflammatory axis compared to amlodipine and hydrochlorothiazide.
