Background This study examined whether targeted disruption of the genes for the prostacyclin receptor (IP) or the thromboxane A 2 receptor (TP) confers a susceptibility to salt-dependent hypertension. Methods and Results Eight female IP-or TP-deficient mice were examined. Baseline systolic blood pressure (SBP) did not differ between TP (-/-) and TP (+/+), but was significantly lower in the IP (-/-) group than in the IP (+/+). With a high salt diet, SBP in IP (-/-) gradually increased. In contrast, SBP in the IP (+/+), TP (-/-), or TP (+/+) groups remained unchanged. Conclusions The prostacyclin receptor may participate in the maintenance of baseline BP. With salt loading, BP adaptation may take place, at least in part, via IP mediated signals.(Circ J 2005; 69: 124-126)