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Angiotensin II (ANG II) plays a key role in regulating blood pressure and inflammation. Prostaglandin E 2  (PGE 2 ) signals through four different G protein-coupled receptors, eliciting a variety of effects. We reported that activation of the EP 3  receptor reduces cardiac contractility. More recently, we have shown that overexpression of the EP 4  receptor is protective in a mouse myocardial infarction model. We hypothesize in this study that the relative abundance of EP 3  and EP 4  receptors is a major determinant of end-organ damage in the diseased heart. Thus EP 3  is detrimental to cardiac function and promotes inflammation, whereas antagonism of the EP 3  receptor is protective in an ANG II hypertension (HTN) model. To test our hypothesis, male 10- to 12-wk-old C57BL/6 mice were anesthetized with isoflurane and osmotic minipumps containing ANG II were implanted subcutaneously for 2 wk. We found that antagonism of the EP 3  receptor using L798,106 significantly attenuated the increase in blood pressure with ANG II infusion. Moreover, antagonism of the EP 3  receptor prevented a decline in cardiac function after ANG II treatment. We also found that 10- to 12-wk-old EP 3 -transgenic mice, which overexpress EP 3  in the cardiomyocytes, have worsened cardiac function. In conclusion, activation or overexpression of EP 3  exacerbates end-organ damage in ANG II HTN. In contrast, antagonism of the EP 3  receptor is beneficial and reduces cardiac dysfunction, inflammation, and HTN.    NEW &amp; NOTEWORTHY This study is the first to show that systemic treatment with an EP 3  receptor antagonist (L798,106) attenuates the angiotensin II-induced increase in blood pressure in mice. The results from this project could complement existing hypertension therapies by combining blockade of the EP 3  receptor with antihypertensive drugs.

The deleterious role of the prostaglandin E2 EP3 receptor in angiotensin II hypertension

The deleterious role of the prostaglandin E₂ EP₃ receptor in angiotensin II hypertension