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SEX DIFFERENCES IN CONSTRICTOR RESPONSES TO BERAPROST IN RAT MESENTERIC ARTERIOLES: ROLES OF THROMBOXANE VS. PGE2 PROSTANOID RECEPTORS
Author(s) -
Sellers Minga,
Stallone John
Publication year - 2011
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.25.1_supplement.1026.35
Subject(s) - constriction , medicine , prostacyclin , endocrinology , prostanoid , antagonist , thromboxane , receptor , thromboxane receptor , chemistry , thromboxane a2 , receptor antagonist , platelet
Recently it was reported that prostacyclin (PGI 2 ) and its analogue beraprost (Bpst) cause constriction in rat aorta, likely via thromboxane receptor (TP). We investigated this effect of Bpst in the microvasculature (rat mesenteric arterioles, MA), as well as the role of PGE 2 receptors (EP) and whether sex differences exist in the constrictor response to Bpst. Male (M) and female (F) Sprague‐Dawley rats (14–16 wks age) were sacrificed and reactivity to Bpst was measured in MA (100–200 μm dia.) using isometric myography. Concentration‐response curves to Bpst (10 −8 – 10 −4 M) were obtained in the presence of indomethacin (INDO, 10 −5 M; COX 1/2 inhibitor) alone or with CAY 10441 (CAY, 10 −6 M; PGI 2 receptor antagonist) and one of the following: SQ 29,548 (SQ, 10 −6 M; TP antagonist) or AH 6809 (AH, 10 −5 M; EP antagonist). In F MA, Bpst caused constriction in all groups; the greatest responses were in INDO+CAY and INDO+CAY+AH, suggesting that TP mediates the constrictor responses to Bpst in F MA. In M MA, Bpst also caused constriction in all groups. While INDO+CAY exhibited the greatest response, INDO+CAY+SQ exhibited significantly greater constriction than INDO alone or INDO+CAY+AH, indicating that in M MA, Bpst produces constriction via EP rather than TP. In conclusion, Bpst produces similar constriction in both M and F MA; however, F appear to rely more upon TP, while M relies more on EP for this constrictor effect. (NIH: HL‐080402)