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Rheumatoid Arthritis Does Not Reduce the Pharmacodynamic Response to Valsartan

From the Faculty of Pharmacy and Pharmaceutical Sciences (N. Daneshtalab, Dr. Jamali) and Faculty of Medicine (Dr. Lewanczuk, Dr. Russell), University of Alberta, Edmonton, Alberta, Canada.

Inflammatory conditions decrease the cardiovascular response to calcium channel and ß-adrenergics blockers due, likely, to down-regulation of the receptors mediated by pro-inflammatory mediators such as C-reactive protein (CRP), nitric oxide (NO), and tumor necrosis factor. The purpose of this investigation was to determine whether down-regulation is also evident in angiotensin II type 1 receptors (AT₁R) during varying inflammatory states. Normotensive subjects were divided into three groups according to the severity of disease: 14 with active rheumatoid arthritis, 12 with controlled rheumatoid arthritis, and 12 healthy control subjects. The AT₁R antagonist valsartan (160 mg) was given to all the subjects, and blood samples were taken for pharmacokinetic analysis. The systolic, diastolic, and mean arterial pressures were determined at all blood collection times. The degree of inflammation was measured using joint swelling, NO, and CRP. Plasma valsartan concentration was measured using high-performance liquid chromatography (HPLC). Patients with active disease had significantly higher joint swelling, NO, and CRP than other groups. Plasma valsartan concentration-time curves were remarkably similar in all groups. No reduced response was noticed. Our preliminary observation suggests a need for further studies to examine the possibility of AT₁R antagonists as alternatives to other cardiovascular drugs so that their potency may be reduced by inflammation.

Key Words: Angiotensin II type 1 receptors • pharmacokinetics • pharmacodynamics • inflammation • rheumatoid arthritis • receptor down-regulation • drug-disease interaction • pro-inflammatory mediators • NO • C-reactive protein

Address for reprints: Dr. F. Jamali, Faculty of Pharmacy and Faculty of Medicine, University of Alberta, Edmonton, Alberta, Canada T6G 2N8.

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