Estrogen replacement in middle-aged women: thermoregulatory responses to exercise in the heat

Tankersley, Clarke G.; Nicholas, W. Channing; Deaver, Daniel R.; Mikita, Da Ja; Kenney, W. L.

doi:10.1152/jappl.1992.73.4.1238

Cited by 102 publications

(83 citation statements)

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“…smaller effect on indices of water and electrolyte metabolism that we observed in response to tamoxifen, compared with those reported in oestrogen-treated women [9,11,12]. It remains to be seen whether the newly-developed anti-oestrogenic agents exhibit similar effects to those of tamoxifen, since the agents within this class of drugs appear to exhibit varying degrees of oestrogenicity at different target tissues.…”

Section: Discussioncontrasting

confidence: 54%

The anti‐oestrogen tamoxifen produces haemodilution in normal postmenopausal women

Grey

Evans

Kyle

et al. 1997

Journal of Internal Medicine

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Abstract. Grey AB, Evans MC, Kyle C, Reid, IR (University of Auckland, Auckland, New Zealand). The anti-oestrogen tamoxifen produces haemodilution in normal postmenopausal women. J Intern Med 1997; 242: 383-8. Objectives.To report the effects of the anti-oestrogen tamoxifen on biochemical and haematological parameters. Design. Randomized, double-blind comparison of tamoxifen 20 mg per day and placebo, over two years. Setting. A university hospital. Subjects. Forty-six healthy late-postmenopausal women (mean, SD time since menopause; 11, seven years). Main outcome measures. Blood specimens were drawn in the fasting state at baseline, six months and two years for measurement of haemoglobin, haematocrit, erythrocyte mean cell volume, mean erythrocyte haemoglobin, leucocyte count, platelet count, urea, electrolytes, creatinine and albumin.Results. There was a significant decline in the haemoglobin concentration in the tamoxifen group (Ϫ4.4, 1.2 g/L; mean, SE) and its levels were lower in this group than in those receiving placebo (P ϭ 0.004). Similarly, haematocrit, erythrocyte count and total leucocyte count were lower in those on placebo (P ϭ 0.002, P ϭ 0.01 and P ϭ 0.01, respectively) and platelet count showed a similar trend (P ϭ 0.08). In the tamoxifen group, the level of serum albumin fell significantly (Ϫ2.2, 0.4 g/L) and was lower throughout the study than that in the placebo group (P ϭ 0.006). That of serum urea tended to fall (Ϫ0.4, 0.2 mmol L) but the between-groups comparison was not significant (P ϭ 0.18). Conclusions. These data suggest that tamoxifen exerts a haemodilutory effect in normal postmenopausal women. Since a similar effect has been reported in response to postmenopausal oestrogen therapy, it is likely that the observed changes represent another oestrogenic effect of tamoxifen in postmenopausal women. Haemodilution may contribute to the reduced incidence of cardiovascular disease reported in tamoxifen-treated women, and, therefore, its assessment in the new oestrogen agonists/antagonists being developed for cardiovascular disease prevention may be important.

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Section: Discussioncontrasting

confidence: 54%

The anti‐oestrogen tamoxifen produces haemodilution in normal postmenopausal women

Grey

Evans

Kyle

et al. 1997

Journal of Internal Medicine

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“…Estrogen-mediated increases in plasma volume are consistent with earlier findings in postmenopausal (2,88) and young women (9,34). The estrogenmediated plasma volume expansion is not always accompanied by changes in water retention, and the mid-luteal phase plasma volume contraction not always associated with greater urine loss.…”

Section: Osmotic Regulation Of Avp and Fluid Balancesupporting

confidence: 89%

“…Sex hormone administration is accompanied by significant water and sodium retention (2, 9), which leads to plasma volume expansion (6, 8,106, 115). In fact, variations in plasma volume at rest and during exercise that are observed following estrogen administration and during different phases of the menstrual cycle are comparable to the reported effects of posture, skin temperature and exercise intensity (43).…”

Section: Protocol A: Sex Hormone Effects On Body Water Regulation Durmentioning

confidence: 99%

Hormonal Contraception, Body Water Balance and Thermoregulation

Stachenfeld¹

2000

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and to the Office of Management and Budget,, Washington, DC 20503 AGENCY USE ONLY (Leave blank)2. REPORT DATE October 2000 REPORT TYPE AND DATES COVEREDAnnual (15 Sep 99 -14 Sep 00) TITLE AND SUBTITLEHormonal Contraception, Body Water Balance and Thermoregulation AUTHOR(S)Nina Stachenfeld, Ph.D. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)The John B Pierce Laboratory New Haven, Connecticut 06519 E-MAIL:nstach@jbpierce.org To test the hypothesis that estrogen enhances water and sodium retention, we compared the fluid regulatory responses to 150 min of exercise-induced dehydration, followed by 180 min of ad libitum drinking during the follicular and luteal phases of the menstrual cycle, and following treatment with an estrogen/progestin (OC EP) and a progestin-only (OC P) oral contraceptive in a double-blind, randomized, cross-over design. We found a downward shift in osmotic regulation of arginine vasopressin (AVP) during the luteal phase and OC EP compared to the follicular phase during exercise, which was not accompanied by plasma volume expansion or fluid retention. Overall fluid and electrolyte balance was similar across all trials. We also determined that the variability of the fluid regulatory hormones (renin, aldosterone and atrial natriuretic peptide) was high over the course of two menstrual cycles, but slopes and intercepts defining osmotic regulation of AVP were highly reliable. We also determined the estrogen and progesterone effects on thermoregulation. OC P increased core temperature and delayed the onset of sweating during exercise, but that OC E+P blocks these effects. This indicates that estrogen blocks the progestin-related changes in thermoregulation. We also found that all of these effects were independent of changes in plasma volume. In our third protocol, we have found that osmotic regulation of thirst is reduced in the luteal phase compared to the follicular phase and to men, without any effects of OC P or OC EP. Fluid balance was unaffected by phase or OCs. We have not completed analysis of the AVP at this point. SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES)U SUBJECT TERMSWomens Health, estrogen, progesterone, body fluid regulation, thermoregulation, sodium regulation, ANP, AVP, PRA, aldosterone INTRODUCTIONMethods to regulate and suppress menstruation and provide contraception are needed as women take more active roles in the military. The administration of estrogen and progestin combinations in...

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“…Therefore, many factors could potentially play a role in the E 2 reduction of T CORE in a supraneutral T AMBIENT . Although the mechanism remains to be determined, these findings are relevant to understanding thermoregulatory dysfunction in menopausal women, who tolerate heat stress better after estrogen replacement therapy (52). We have previously shown that KNDy neurons are required for the rise in LH secretion after the removal of E 2 negative feedback (11).…”

Section: Discussionmentioning

confidence: 95%

Role for kisspeptin/neurokinin B/dynorphin (KNDy) neurons in cutaneous vasodilatation and the estrogen modulation of body temperature

Mittelman-Smith

Williams

Krajewski-Hall

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

165

110

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Estrogen withdrawal in menopausal women leads to hot flushes, a syndrome characterized by the episodic activation of heat dissipation effectors. Despite the extraordinary number of individuals affected, the etiology of flushes remains an enigma. Because menopause is accompanied by marked alterations in hypothalamic kisspeptin/neurokinin B/dynorphin (KNDy) neurons, we hypothesized that these neurons could contribute to the generation of flushes. To determine if KNDy neurons participate in the regulation of body temperature, we evaluated the thermoregulatory effects of ablating KNDy neurons by injecting a selective toxin for neurokinin-3 expressing neurons [NK 3 -saporin (SAP)] into the rat arcuate nucleus. Remarkably, KNDy neuron ablation consistently reduced tail-skin temperature (T SKIN ), indicating that KNDy neurons facilitate cutaneous vasodilatation, an important heat dissipation effector. Moreover, KNDy ablation blocked the reduction of T SKIN by 17β-estradiol (E 2 ), which occurred in the environmental chamber during the light phase, but did not affect the E 2 suppression of T SKIN during the dark phase. At the high ambient temperature of 33°C, the average core temperature (T CORE ) of ovariectomized (OVX) control rats was significantly elevated, and this value was reduced by E 2 replacement. In contrast, the average T CORE of OVX, KNDy-ablated rats was lower than OVX control rats at 33°C, and not altered by E 2 replacement. These data provide unique evidence that KNDy neurons promote cutaneous vasodilatation and participate in the E 2 modulation of body temperature. Because cutaneous vasodilatation is a cardinal sign of a hot flush, these results support the hypothesis that KNDy neurons could play a role in the generation of flushes.reproduction | gonadotropin-releasing hormone | thermoregulation E strogen withdrawal leads to hot flushes in the majority of menopausal women (1). Hot flushes are also experienced by men and women treated with tamoxifen for breast cancer, men undergoing androgen-ablation therapy for prostate cancer, young oophorectomized women, and hypogonadal men (2, 3). A hot flush is characterized by episodic activation of heat dissipation effectors, including cutaneous vasodilatation, sweating, and behavioral thermoregulation. After a flush is initiated, the activation of heat dissipation mechanisms is so effective that core temperature frequently drops (4). Despite the vast numbers of individuals affected, the etiology of flushes remains an enigma.Hot flushes are closely timed with luteinizing hormone (LH) pulses, providing a clue that the generation of flushes is linked to the hypothalamic neural circuitry controlling pulsatile gonadotropin-releasing hormone (GnRH) secretion (5, 6). Current evidence suggests that pulsatile GnRH secretion is modulated by a subpopulation of neurons in the arcuate (infundibular) nucleus that express estrogen receptor α (ERα), neurokinin 3 receptor (NK 3 R), kisspeptin, neurokinin B (NKB), and dynorphin (7-11). In the hypothalamus of postmenopausal women, ...

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Estrogen replacement in middle-aged women: thermoregulatory responses to exercise in the heat

Cited by 102 publications

References 0 publications

The anti‐oestrogen tamoxifen produces haemodilution in normal postmenopausal women

The anti‐oestrogen tamoxifen produces haemodilution in normal postmenopausal women

Hormonal Contraception, Body Water Balance and Thermoregulation

Role for kisspeptin/neurokinin B/dynorphin (KNDy) neurons in cutaneous vasodilatation and the estrogen modulation of body temperature

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