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Cutaneous Vascular and Sweating Responses to Intradermal Administration of Prostaglandin E1 and E2 in Young and Older Adults: a Role for Nitric Oxide?
Author(s) -
Fujii Naoto,
Singh Maya Sarah,
Halili Lyra,
Boulay Pierre,
Sigal Ronald J,
Kenny Glen P
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.1290.2
Subject(s) - vasodilation , medicine , nitric oxide , prostaglandin e2 , sweat , prostaglandin e1 , endocrinology , ageing , young adult , forearm , surgery
Cyclooxygenase (COX) contributes to cutaneous vasodilation and sweating responses, however the mechanisms underpinning these responses remain unknown. We hypothesized that prostaglandin E1 (PGE1) and E2 (PGE2), which are COX‐derived products, directly mediate cutaneous vasodilation and sweating through nitric oxide synthase (NOS)‐dependent mechanisms in young adults. Furthermore, we hypothesized that this response is diminished in older adults, since ageing attenuates COX‐dependent cutaneous vasodilation and sweating. In 9 young (4 males and 5 females, 22 ± 5 years) and 10 older (3 males and 7 females, 61 ± 4 years) adults, cutaneous vascular conductance (CVC, laser‐Doppler perfusion units/mean arterial pressure) and sweat rate (ventilated capsule) were measured at four intradermal forearm skin sites receiving incremental doses (0.05, 0.5, 5, 50, 500 μ M each for 25 min) of PGE1 or PGE2 with and without co‐administration of 10 m M L ‐NNA, a non‐specific NOS inhibitor. L ‐NNA attenuated PGE1‐mediated increases in CVC in young adults, while it attenuated PGE2‐mediated increases in CVC in older adults (all P < 0.05). However, the magnitude of the PGE1‐ and PGE2‐mediated increases in CVC did not differ between groups (all P > 0.05). Neither PGE1 nor PGE2 increased sweat rate at any of the administered concentrations for either the young or older adults (all P > 0.05). We show that the cutaneous vasodilator response is mediated through NOS‐dependent mechanisms albeit via PGE1 in young adults and PGE2 in older adults, respectively. We also show that cutaneous vascular responsiveness to PGE1 and PGE2 is similar between young and older adults. Lastly, in both young and older adults, we show that both PGE1 and PGE2 do not directly increase sweat rate. Support or Funding Information This study was supported by the Natural Sciences and Engineering Research Council of Canada (Discover grant, RGPIN‐06313‐2014; Discovery Grants Program ‐ Accelerator Supplement, RGPAS‐462252‐2014), and by Canada Foundation for Innovation (Leaders Opportunity Fund, 22529) (funds held by Dr. Glen P. Kenny).