(A) Reduced pressor response to Ang II in EP1^–/– versus EP1^+/+ mice. MAP was recorded by intracarotid arterial monitoring before and during i.v. infusion of Ang II (75 pmol/kg/min). n = 8 per group. ***P < 0.005. (B) The pressor response to Ang II integrated over time was significantly reduced in EP1^–/– compared with EP1^+/+ mice. AUC, area under the curve. **P < 0.01. (C) Effect of chronic Ang II infusion (1,000 ng/kg/min) on systolic blood pressure determined by tail cuff. Baseline blood pressure was significantly lower in EP1^–/– mice than in EP1^+/+ mice (n = 5 per group) and the difference between genotypes increased following Ang II infusion. ***P < 0.001; ****P < 0.0001. (D) The change in systolic blood pressure following Ang II minipump was significantly greater in EP1^+/+ than in EP1^–/– mice (n = 5). ****P < 0.0001. (E) MAP determined by intracarotid catheterization was significantly greater in EP1^+/+ (n = 3) than in EP1^–/– (n = 4) mice infused with Ang II. *P < 0.05. (F) Expression of EP1 receptor mRNA in microdissected mouse mesenteric arteries and aortic tissue. Lack of RT was utilized as a negative control and β-actin served as RNA loading control. (G) Reduced constriction of Ang II on in vitro mesenteric arteriolar rings following pretreatment with the EP1 receptor antagonist SC51322. n = 7 per group. (H) Reduced Ang II constriction of preglomerular arterioles following treatment with EP1 receptor antagonist SC51322 (1 μM). n = 7 per group. *P < 0.005.