Altered reflex control of cutaneous circulation by female sex steroids is independent of prostaglandins

We tested the hypothesis that the shift in the cutaneous vasodilator respon se to hyperthermia seen with elevated female reproductive hormones is a pro staglandin-dependent resetting of thermoregulation to higher internal tempe ratures, similar to that seen in the febrile response to bacterial infectio n. Using water-perfused suits to control body temperature, we conducted hea t stress experiments in resting women under conditions of low and high prog esterone and estrogen and repeated these experiments after an acute dose of ibuprofen (800 mg). In six women the hormones were exogenous (oral contrac eptives); three women had regular menstrual cycles and were tested in the e arly follicular and midluteal phases. Resting oral temperature (T-or) was s ignificantly elevated with high hormone status (P < 0.05); this was not aff ected by ibuprofen treatment (P > 0.2). The T-or threshold for cutaneous va sodilation was significantly increased by high hormone status (+0.27 +/- 0. 07 degrees C, P < 0.02); the shift was not affected by ibuprofen treatment (with ibuprofen: +0.29 +/- 0.08 degrees C, P > 0.2 vs. control experiments) . The T-or threshold for sweating was similarly increased by high hormone s tatus (+0.22 +/- 0.05 degrees C, P < 0.05); this shift was not influenced b y ibuprofen (with ibuprofen: +0.35 +/- 0.05, P > 0.1 vs. control experiment s). Thus the shift in thermoregulatory control of skin blood flow and sweat ing mediated by female reproductive steroids is not sensitive to ibuprofen; it therefore appears that this shift is independent of prostaglandins.