Nisha Charkoudian

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 response to hyperthermia seen with elevated female reproductive hormones is a prostaglandin-dependent resetting of thermoregulation to higher internal temperatures, similar to that seen in the febrile response to bacterial infection. Using water-perfused suits to control body temperature, we conducted heat stress experiments in resting women under conditions of low and high progesterone and estrogen and repeated these experiments after an acute dose of ibuprofen (800 mg). In six women the hormones were exogenous (oral contraceptives); three women had regular menstrual cycles and were tested in the early follicular and midluteal phases. Resting oral temperature (Tor) was significantly elevated with high hormone status ( P < 0.05); this was not affected by ibuprofen treatment ( P > 0.2). The Tor threshold for cutaneous vasodilation was significantly increased by high hormone status (+0.27 ± 0.07°C, P < 0.02); the shift was not affected by ibuprofen treatment (with ibuprofen: +0.29 ± 0.08°C, P > 0.2 vs. control experiments). The Torthreshold for sweating was similarly increased by high hormone status (+0.22 ± 0.05°C, P < 0.05); this shift was not influenced by ibuprofen (with ibuprofen: +0.35 ± 0.05, P > 0.1 vs. control experiments). Thus the shift in thermoregulatory control of skin blood flow and sweating mediated by female reproductive steroids is not sensitive to ibuprofen; it therefore appears that this shift is independent of prostaglandins.We tested the hypothesis that the shift in the cutaneous vasodilator response to hyperthermia seen with elevated female reproductive hormones is a prostaglandin-dependent resetting of thermoregulation to higher internal temperatures, similar to that seen in the febrile response to bacterial infection. Using water-perfused suits to control body temperature, we conducted heat stress experiments in resting women under conditions of low and high progesterone and estrogen and repeated these experiments after an acute dose of ibuprofen (800 mg). In six women the hormones were exogenous (oral contraceptives); three women had regular menstrual cycles and were tested in the early follicular and midluteal phases. Resting oral temperature (Tor) was significantly elevated with high hormone status (P < 0.05); this was not affected by ibuprofen treatment (P > 0.2). The Tor threshold for cutaneous vasodilation 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 Tor threshold for sweating was similarly increased by high hormone status (+0.22 +/- 0.05 degrees C, P < 0.05); this shift was not influenced by ibuprofen (with ibuprofen: +0.35 +/- 0. 05, P > 0.1 vs. control experiments). Thus the shift in thermoregulatory control of skin blood flow and sweating mediated by female reproductive steroids is not sensitive to ibuprofen; it therefore appears that this shift is independent of prostaglandins.

The Complex Challenge of Blood Pressure Regulation

Abstract The regulation of arterial pressure is one of the most complex and integrative phenomena in human physiology. Central to this regulation is the sympathetic nervous system, which controls vascular tone, cardiac chronotropy and inotropy, and modulates renal and adrenal hormonal responses. Importantly, sympathetic regulation of arterial pressure is very different between men and women. In younger healthy people, women tend to have lower blood pressure and lower sympathetic neural activity compared to men. As a result, women have lower risk of hypertension and other cardiovascular diseases until around the age of menopause. After menopause, the risk of hypertension and its associated comorbidities increases sharply in women, and can be even greater than that in men (although risk of hypertension increases with each decade of age in both sexes). In this chapter, our goal is to a brief clinical update of mechanisms contributing to arterial pressure regulation in healthy men and women, and how these mechanisms change with age, menopause, and development of hypertension.