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The early postmenopausal phase is associated with a decline in vascular function: is the prostanoid system to blame?
Author(s) -
Nyberg Michael,
Egelund Jon,
Nielsen Mads Bernhard,
Mogensen Alexander,
Hellsten Ylva
Publication year - 2016
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.30.1_supplement.957.5
Subject(s) - prostacyclin , medicine , menopause , prostanoid , vasodilation , vasomotor , endocrinology , iloprost , prostaglandin
Menopause is associated with a decline in vascular function; however, whether this is an effect of age and/or menopause and the mechanisms underlying this decline remains unclear. We examined the vascular response to femoral arterial infusion of vasoactive compounds in 20 pre‐and 17 recent postmenopausal women of similar age (49±2 vs. 53±2 years). The postmenopausal women had not experienced a menstrual cycle during the previous 12 months but were less than 5 years past their final menstrual period (2.9±0.6 years). The change in leg vascular conductance (LVC) in response to infusion of the endothelium‐dependent vasodilator acetylcholine (ACh) was lower (~25%, P <0.05) in the postmenopausal compared to the premenopausal women. Co‐infusion of ketorolac to inhibit prostanoid formation reduced the vasodilator response to ACh to a similar extent in the two groups of women. Despite the similar effect of ketorolac, the change in LVC with infusion of the prostacyclin analog epoprostenol was lower (~40%, P <0.05) in the postmenopausal compared to the premenopausal women. These findings suggest that vascular function is adversely altered already within the first years following menopause. The early onset of this altered function indicates that this change is more related to menopausal status than aging per se . The reduced endothelial function does not appear to be related to an altered function of the prostanoid system despite a reduced vascular sensitivity to prostacyclin. Support or Funding Information Financial support for the study was provided by the faculty of SCIENCE at University of Copenhagen.