Key result
COX-1-derived PGE2 signaling through EP1R in the subfornical organ is required for ROS-mediated hypertension induced by systemic infusion of Angiotensin II in mice.
Population
Mice models including wild-type, EP(1)R(-/-), COX-1(-/-), and COX-2(-/-) mice
Comparison
Systemic infusion of slow-pressor doses of… vs Wild-type mice or baseline conditions
Design
Preclinical
Authors
Loading...
Suggests EP1R as a novel target in Ang II hypertension; leaves open translation to human therapy.
COX-1-derived PGE2 signaling through EP1 receptors in the subfornical organ is essential for Angiotensin II-dependent hypertension, highlighting a potential novel therapeutic target.
Cao et al. (2012) studied Angiotensin II-dependent hypertension. EP1R antagonist SC-51089 and genetic reconstitution of EP1R vs. Wild-type or null mutation controls was evaluated on Blood pressure (hypertension) and ROS formation. COX-1-derived PGE2 signaling through EP1R in the subfornical organ is required for ROS-mediated hypertension induced by systemic infusion of Angiotensin II in mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: