Hydrochlorothiazide increases interleukin-1 beta (IL-1β) secretion by peripheral blood mononuclear cells in healthy subjects

Abstract

Recent study shows close relationship between hypertension and inflammation. The concentration of inflammatory mediators is increased in patients with essential hypertension. Angiotensin II (Ang II) may contribute to inflammatory process. Previous studies showed that individuals with essential hypertension had increased interleukin-1beta (IL-1β) secretion by peripheral blood mononuclear cells (PBMCs) and also valsartan and simvastatin reduced this inflammatory marker. In this study, the effect of hydrochlorothiazide on IL-1β secretion by PBMCs in healthy subjects was investigated. PBMCs in healthy subjects were isolated by gradient centrifugation. After incubation with Ang II and hydrochlorothiazide, IL-1 β concentrations in supernatant from PBMCs were measured by enzymelinked immunosorbent assay (ELISA). When compared with the control group, hydrochlorothiazide (10^-8, 10^-9 M) increased secretion of IL-1β from PBMCs after stimulation by Ang II. Hydrochlorothiazide may increase inflammatory mediator secretion from PBMCs.

Key words: Hydrochlorothiazide, hypertension, interleukin-1 beta, peripheral blood mononuclear cells (PBMCs).