Rheumatoid arthritis does not reduce the pharmacodynamic response to valsartan.

Inflammatory conditions decrease the cardiovascular response to calcium channel and beta-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 (AT(1)R) 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 AT(1)R 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 AT(1)R antagonists as alternatives to other cardiovascular drugs so that their potency may be reduced by inflammation.