Effects of Salt Loading on Blood Pressure in Mice Lacking the Prostanoid Receptor Gene

International Union of Basic and Clinical Pharmacology. LXXXIII: Classification of Prostanoid Receptors, Updating 15 Years of Progress

“…Francois et al (2005) found that IP-deficient mice fed on a high-salt (6% NaCl) diet developed a significantly larger increase in blood pressure than wild-type mice without alteration in renin and aldosterone levels, and concomitantly developed cardiac hypertrophy and fibrosis. Their finding on saltinduced hypertension in IP(Ϫ/Ϫ) is consistent with that of Watanabe et al (2005), who found that with a highsalt diet, systolic blood pressure in female IP(Ϫ/Ϫ) mice gradually increased, whereas that in the IP(ϩ/ϩ), TP(Ϫ/Ϫ), or TP(ϩ/ϩ) mice remained unchanged. On the other hand, Hara et al (2005) examined cardiac hypertrophy and fibrosis in response to pressure overload.…”

Cyclooxygenases, microsomal prostaglandin E synthase-1, and cardiovascular function

“…While deletion of the IP augments the response to thrombogenic or hypertensive stimuli, depression of PGE 2 might also influence cardiovascular function. Thus, deletion of the EP2 receptor (25), like that of the IP (22,26), increases salt sensitivity in mice. In addition to effects on blood pressure, low con- centrations of PGE 2 activate platelets via the EP3, while higher concentrations inhibit platelet function by ligating the IP (27).…”

Prostacyclin Stimulated Integrin-Dependent Angiogenic Effects of Endothelial Progenitor Cells and Mediated Potent Circulation Recovery in Ischemic Hind Limb Model

“…IP -/-mice with the genetic background of C57BL/6 were prepared as described previously. 18 For cell tracing experiments, green fluorescent protein (GFP) transgenic mice (C57BL/6, homozygous) donated by M. Okabe (Osaka University, Japan) were used. BM transplantation models in which BM mononuclear cells (BM-MNCs) from wildtype (WT) and IP -/-mice were injected into WT or IP -/-mice were established as described previously.…”