Premium
Angiotensin II receptor synergism with prostaglandin E 2 receptors
Author(s) -
Palazzo Maria C.,
Breyer Richard M
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.880.5
Subject(s) - vasoconstriction , angiotensin ii , angiotensin ii receptor type 1 , chemistry , endocrinology , medicine , prostaglandin , renin–angiotensin system , receptor , aldosterone , pharmacology , phenylephrine , rho associated protein kinase , angiotensin receptor , long term potentiation , blood pressure , signal transduction , biochemistry
Upon intravenous infusion prostaglandin E 2 (PGE 2 ) acts as a systemic vasodepressor in mice and humans. Under certain circumstances however PGE 2 may act as a vasopressor. Subthreshold concentrations of vasoconstrictors such as potassium chloride or phenylephrine enhance PGE 2 ‐mediated vasoconstriction. Here we demonstrate using wire myography that angiotensin II (Ang II), a principal effector of the renin‐angiotensin‐ aldosterone‐system, potentiates PGE 2 ‐mediated vasoconstriction in mouse femoral arteries. Using knockout mice and pharmacological inhibitors, we have determined that this potentiation effect is mediated via the angiotensin AT1 receptor and the PGE 2 EP3 receptor. Y‐27632, a Rho kinase inhibitor, blocked the Ang II‐evoked potentiation of EP3 action suggesting a role for the Rho‐ROCK pathway in the observed potentiation. Our data support the hypothesis that angiotensin II synergizes with PGE 2 to induce vasoconstriction. The significance on blood pressure homeostasis and detailed mechanism of this interaction remains to be determined. This work was supported by a grant from the NIH NIDDK DK37097(RMB)