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Sex differences in fractalkine responses in spontaneously hypertensive rats (SHR)
Author(s) -
Pardieck Jennifer Lynn,
Sullivan Jennifer C,
Pollock Jennifer S
Publication year - 2007
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.21.6.a1418
Subject(s) - mesenteric arteries , incubation , acetylcholine , medicine , endocrinology , receptor , biology , artery , biochemistry
Lower cardiovascular risk in females has been linked to a sex difference in NO bioavailability. Fractalkine (FKN) has been shown to stimulate NOS to produce NO. We designed experiments to test the hypothesis that females have greater FKN‐stimulated, NOS‐mediated vasorelaxation. The mesenteric arterial bed (MAB) was isolated for measurement of FKN by RT‐PCR and for FKN ligand and receptor by Western blot. Third order mesenteric arteries from male and female SHR (12–14 weeks) were isolated, and a cumulative dose‐response curve was performed to acetylcholine (Ach) in arteries pre‐incubated with FKN (1μg/mL) or vehicle in the absence or presence of the NOS inhibitor N ω ‐nitro‐L‐arginine methyl ester (LNAME; 100 μM). There was greater FKN expression in the MAB of females when measured by RT‐PCR (RDU: males, 0.2±0.1; females, 2.2±0.5, p=0.02), but FKN ligand and receptor protein expression were similar. LNAME produced a similar decrease in sensitivity and maximum response to Ach in arteries from males and females. Pre‐incubation with FKN alone did not alter Ach‐induced relaxation; however, incubation with FKN and LNAME produced a greater decrease in maximum response in males compared to females. These data suggest that despite increased FKN mRNA in arteries from females, FKN potentiates Ach‐stimulated NO production to a greater extent in arteries from males. Funded by HL60653, HL64776, and AHA.