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Indomethacin enhances reactivity to vasopressin in normotensive and hypertensive rats, while PGE 2 receptor blockade only attenuates reactivity in normotensive rats.
Author(s) -
Sellers Minga M,
Stallone John N
Publication year - 2010
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.24.1_supplement.982.14
Subject(s) - medicine , endocrinology , vasopressin , thromboxane , prostacyclin , receptor , receptor antagonist , antagonist , chemistry , thromboxane receptor , platelet
Previously, we reported that in female (F) rats 17‐β‐estradiol and aortic coarctation‐induced hypertension (ACIH) increase release of thromboxane (TXA 2 ) and prostacyclin from mesenteric arterioles (MA), and that constrictor responses of aorta to vasopressin (VP) are reduced ~40% by TP receptor antagonist SQ 29,548 (SQ). Thus, the roles of TXA 2 and PGE 2 in constrictor responses to VP were studied in MA. F Sprague‐Dawley rats (14–16 wks age) underwent ACIH (hypertensive; HT) or sham (normotensive; NT). Rats were sacrificed 12–14 days post‐ACIH and reactivity to VP was measured in MA (150–200 μm dia.) using isometric myography. Data are means ± S.E. (n = 4–5 rats/group). Maximal contractile responses of MA to VP did not differ between NT (9.97 ± 0.75 mN/mm) and HT (11.77 ± 1.40). SQ (40 μM) did not alter responses in NT (9.16 ± 1.53) or HT (12.69 ± 1.77). In separate rats, maximal responses to VP did not differ between NT and HT. AH6809, a PGE 2 receptor blocker (EP1, 2, 3) reduced maximal responses of MA from NT (8.95 ± 0.36 vs. 10.24 ± 0.63) but not HT (9.73 ± 0.81 vs. 9.36 ± 0.61). Indomethacin (non‐specific COX inhibitor; 10 μM) increased contractions to VP in NT and HT (11.74 ± 0.84 and 12.75 ± 0.79, respectively). While TXA 2 potentiates constrictor responses of aorta to VP, the role of TXA 2 in reactivity of MA to VP is less certain. However, it appears that PGE 2 may also play a role in modulating MA responses to VP in NT rats. (NIH:HL‐080402)