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Contributions of cyclooxygenase (COX) and NO synthase (NOS) pathways to endothelium‐dependent dilatation in the finger of women
Author(s) -
Marshall Janice Mary
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.1125.5
Subject(s) - cyclooxygenase , acetylcholine , nitric oxide synthase , medicine , endocrinology , vasodilation , chemistry , endothelium , enzyme , nitric oxide , biochemistry
We tested the roles of COX and NOS in finger vasodilatation evoked by iontophoresis of acetylcholine (ACh), using laser Doppler fluximetry. In 12 women in the low oestrogen (E 2 ) phase of the menstrual cycle, aspirin (600mg p.o) decreased baseline finger red cell flux (RCF) from 55.0±7.8 to 30.6±5.5* perfusion units (pu; *: P<0.05), and the ACh‐evoked response from +296.8±23.9 to +251.4±24.4* pu. In the high E 2 phase, COX inhibition decreased baseline from 68.0 ± 13.8 to 38.4 ± 8.1*, but had no effect on the ACh response (259.5±27.4 vs 251.2±23.3 pu). On different days, NOS inhibition with L‐NAME had no effect on baseline RCF in the low, or high E 2 phase. In the low E 2 phase, the ACh response was unchanged (+228.26±25.8 vs 225.6±21.3pu), but aspirin then decreased the response further to 175.9±17.6*pu. In the high E 2 phase, L‐NAME increased the ACh response from +198.1±23.7 to +229.2±27.4*pu; COX inhibition restored it to +202.8±27.8pu. We propose that in the finger, NOS generates both NO and O 2 − and thereby, ONOO − which inhibits PGI 2 synthase. E 2 facilitates NOS and PGI 2 synthase such that when E 2 is high, PGI 2 contributes to endothelium‐dependent finger dilatation only after NOS inhibition.