
doi: 10.1253/circj.69.124
pmid: 15635218
This study examined whether targeted disruption of the genes for the prostacyclin receptor (IP) or the thromboxane A2 receptor (TP) confers a susceptibility to salt-dependent hypertension.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.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.
Mice, Knockout, Heterozygote, Reverse Transcriptase Polymerase Chain Reaction, Body Weight, Homozygote, Blood Pressure, Sodium, Dietary, Receptors, Epoprostenol, Receptors, Thromboxane A2, Prostaglandin H2, Mice, Inbred C57BL, Thromboxane B2, Mice, Heart Rate, Animals, Female
Mice, Knockout, Heterozygote, Reverse Transcriptase Polymerase Chain Reaction, Body Weight, Homozygote, Blood Pressure, Sodium, Dietary, Receptors, Epoprostenol, Receptors, Thromboxane A2, Prostaglandin H2, Mice, Inbred C57BL, Thromboxane B2, Mice, Heart Rate, Animals, Female
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