Influence of progestin bioactivity on cutaneous vascular responses to passive heating.
OBJECTIVE
Oral contraceptives influence the regulation of cutaneous vascular tone, and both estrogen and progesterone have been shown to affect nitric oxide (NO)-mediated vasodilation. We tested the hypothesis that cutaneous vascular conductance (CVC) during passive heating would be lower in women taking oral contraceptives with higher progestational bioactivity compared with those taking oral contraceptives with lower progestational bioactivity. We further hypothesized that this difference could be attributed to the relative degree of NO-dependent vasodilation.


METHODS
Fourteen women (20.3 +/- 0.3 yr) taking combined oral contraceptives (low progestin: 6 subjects, high progestin: 8 subjects) participated in a whole-body heating protocol and were tested during the end of active and placebo pill phases. Red blood cell (RBC) flux was measured by laser-Doppler flowmetry at a control microdialysis site (Ringer's solution) and an experimental site where NO-synthase (NOS) was inhibited (10 mM L-NAME). CVC was calculated as RBC flux/MAP.


RESULTS
Baseline oral temperature (Tor) was significantly higher during the active pill phase for all subjects (active: 36.8 +/- 0.1 degrees C; placebo: 36.6 +/- 0.1 degrees C) (P = 0.02) but was not affected by progestational bioactivity. CVC at the control site during heating did not differ between low and high progestin users during either phase of oral contraceptive use. However, CVC in the NOS inhibited site was diminished during both phases of oral contraceptive use in the low progestin group at a given change in Tor (active: DeltaT(or) of 0.6-1.0 degrees C, placebo: DeltaT(or) of 0.8-1.0 degrees C) (P < 0.05). (DeltaT(or) 1.0 degree C: active: 30.86 vs 46.56%CVC(max); placebo: 26.29 vs 49.22% CVC(max)) (P < 0.05).


CONCLUSIONS
Progestational activity in oral contraceptives may alter the mechanisms by which skin blood flow increases during passive heating via NO-dependent cutaneous active vasodilation.
Houghton
Belinda L
BL
Department of Human Physiology, University of Oregon, Eugene, OR, USA.
Holowatz
Lacy A
LA
Minson
Christopher T
CT
D000328:Adult; D001682:Biological Availability; D001831:Body Temperature / Q000187:drug effects*; D003278:Contraceptives, Oral, Hormonal / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D006801:Humans; D017078:Laser-Doppler Flowmetry; D010919:Placebos; D011372:Progestins / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology*; D012039:Regional Blood Flow / Q000187:drug effects; D012867:Skin / Q000098:blood supply*
D003278:Contraceptives, Oral, Hormonal; D004967:Estrogens; D010919:Placebos; D011372:Progestins