In the present issue of Acta Physiologica, Guan et al. in their article “Mechanisms of sphingosine-1-phosphate-mediated vasoconstriction of rat afferent arterioles” 1 address the signaling events associated with sphingosine-1-phosphate (S1P)-mediated renal afferent vasoconstriction and show in, technically demanding, blood-perfused juxtamedullary nephron preparation that S1P signaling relies predominantly on transmembrane calcium influx from the extracellular fluid through L-type calcium channels with contribution from oxidative stress metabolites1. So not only is new information on S1P signaling of potential therapeutic relevance obtained but the general concept is confirmed that renal preglomerular vascular reactivity relies significantly on calcium influx through voltage gated calcium channels. Authors showed previously, that S1P caused selective renal afferent but not efferent vasoconstriction2 and in conjunction with increased S1P release in pathophysiological situations like sepsis and ischemia-reperfusion incidents, this effect could be relevant in acute kidney injury with parallel decreases in renal blood flow and GFR. This article is protected by copyright. All rights reserved.