Cardiovascular effects of inflammatory interleukins (IL) have been suggested to be mediated by the renin-angiotensin system in vivo. To address the direct cellular effect of IL, we examined the influence of IL-1β on renin secretion and renin mRNA in cultures of mouse juxtaglomerular granular (JG) cells and in the mouse tumor cell line As4.1, which expresses renin mRNA. Renin mRNA levels and secretion of active renin were not significantly changed by IL-1β in native JG cells. Activation of adenylyl cyclase by forskolin increased renin secretion and renin mRNA levels three- and fivefold, respectively. These stimulatory responses to forskolin were not altered by IL-1β. In contrast to native JG cells, renin mRNA abundance was markedly suppressed by IL-1β in As4.1 cells, whereas secretion of active renin and the stability of renin mRNA were not changed. In As4.1 cells forskolin did not change renin secretion or renin mRNA abundance in the absence or in the presence of IL-1β. These findings suggest that IL-1β has no direct influence on renin secretion and renin mRNA abundance at the level of native JG cells.