The Menstrual Cycle and Raynaud's Phenomenon

Greenstein, D.; Jeffcote, N.; Ilsley, D.W.; Kester, R. C.

doi:10.1177/000331979604700501

Cited by 33 publications

(23 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Female patients with Raynaud phenomenon show altered regulation of skin perfusion during the menstrual cycle. 18 As stimulation of endogenous estrogens leads to a potentiation of postischemic skin blood flow, the present results are in line with a major role of estrogens in the regulation of skin perfusion and thermoregulation. [19][20][21] Such an important regulator function helps to explain alterations in thermoregulation of the skin in postmenopausal versus premenopausal women, which is often responsive to estrogen replacement therapy.…”

Section: Discussionsupporting

confidence: 87%

Endogenous Estrogens Increase Postischemic Hyperemia in the Skin Microcirculation

Stojanović

Küng²,

Spieker³

et al. 2005

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

Estrogens have been recognized as a major regulator of vascular tone and structure, particularly in the skin. The objective of this study was to investigate the effects of endogenous estrogens on the skin microcirculation. Skin blood flow was measured at the forearm at rest and during postischemic hyperemia using laser Doppler flowmetry in 32 healthy women (mean age 34.5 ± 3.9 years) involved in an in-vitro fertilization program. Women were treated for 10 to 12 days with gonadotropin-releasing hormone agonist (total dose 40.3 ± 3.3 mg) and human menopausal gonadotropin (1942 ± 801 IE) or follicle-stimulating hormone (2544 ± 1071 IE) according to individual estrogen levels. Plasma estrogen levels increased from 132 ± 90 pmol/L (36 ± 25 pg/mL) to 8471 ± 4386 pmol/L (2308 ± 1195 pg/mL) during treatment (P < 0.0001). Maximal hyperemic blood flow increased from 353 ± 81% before treatment to 516 ± 144% after hormonal stimulation (P < 0.0001), whereas basal skin flow was not altered. This study shows that endogenous estrogens enhance the postischemic hyperemic response of the skin microcirculation.

show abstract

Section: Discussionsupporting

confidence: 87%

Endogenous Estrogens Increase Postischemic Hyperemia in the Skin Microcirculation

Stojanović

Küng²,

Spieker³

et al. 2005

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

show abstract

“…One potential explanation is that continuous administration of exogenous E 2 is more cardioprotective than endogenous, cyclically released E 2 . Continuous E 2 administration may avoid an estrogen withdrawal phenomenon, which has been implicated in the worsening of other vascular diseases during menstruation (17,38,42). Furthermore, OVX may eliminate potentially detrimental sex hormones or estrogen metabolites that may counteract beneficial effects of endogenous E 2 in intact females; E 2 repletion after OVX may thus allow for unopposed E 2 signaling.…”

Section: Discussionmentioning

confidence: 99%

17β-Estradiol mediates superior adaptation of right ventricular function to acute strenuous exercise in female rats with severe pulmonary hypertension

Lahm

Frump

Albrecht

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Since acute exercise-induced increases in afterload may lead to RV dysfunction in PAH, we sought to determine whether E2 allows for superior RV adaptation after an acute exercise challenge. We studied echocardiographic, hemodynamic, structural, and biochemical markers of RV function in male and female rats with sugen/hypoxia (SuHx)-induced pulmonary hypertension, as well as in ovariectomized (OVX) SuHx females, with or without concomitant E2 repletion (75 g·kg Ϫ1 ·day Ϫ1 ) immediately after 45 min of treadmill running at 75% of individually determined maximal aerobic capacity (75% aerobic capacity reserve). Compared with males, intact female rats exhibited higher stroke volume and cardiac indexes, a strong trend for better RV compliance, and less pronounced increases in indexed total pulmonary resistance. OVX abrogated favorable RV adaptations, whereas E 2 repletion after OVX markedly improved RV function. E2's effects on pulmonary vascular remodeling were complex and less robust than its RV effects. Postexercise hemodynamics in females with endogenous or exogenous E 2 were similar to hemodynamics in nonexercised controls, whereas OVX rats exhibited more severely altered postexercise hemodynamics. E 2 mediated inhibitory effects on RV fibrosis and attenuated increases in RV collagen I/III ratio. Proapoptotic signaling, endothelial nitric oxide synthase phosphorylation, and autophagic flux markers were affected by E 2 depletion and/or repletion. Markers of impaired autophagic flux correlated with endpoints of RV structure and function. Endogenous and exogenous E 2 exerts protective effects on RV function measured immediately after an acute exercise challenge. Harnessing E 2's mechanisms may lead to novel RV-directed therapies.sugen/hypoxia; fibrosis; apoptosis; endothelial nitric oxide synthase; autophagy PULMONARY ARTERIAL HYPERTENSION (PAH) is a sexually dimorphic disease with a female-to-male ratio of up to 4:1 (3). Despite availability of 14 Food and Drug Administrationapproved medications, PAH remains a devastating, progressive, and incurable disease, evidenced by the disappointing 3-yr survival rate of only 55% (22). Even though both female sex and right ventricular (RV) function are major determinants of survival in PAH (5, 22, 23), no RV-or sex steroid-directed therapies exist. This is of importance, since women, despite being more prone to PAH development, exhibit better survival than male patients, a phenomenon attributed, at least in part, to better RV function in women (22,23,26,34,62).We and others demonstrated that the female sex hormone 17␤-estradiol (E 2 ) exerts protective effects on RV function in experimental PAH (11,36,37,60), findings that support observations made in healthy postmenopausal hormone replacement therapy users, where circulating E 2 levels correlate with better RV ejection fraction (61). Given the superior RV function of female PAH patients (23, 26), the exquisite sensitivity of the RV to increases in afterload (19), and the recent observation that exercise and physical activity...

show abstract

“…Also, in the uterine artery of diestrous day 1 female rats, ACh activates only EDHF-mediated relaxation, while in estrous, diestrous, day 2, and proestrous rats, ACh releases both EDHF and NO (Dalle Lucca et al, 2000b). The effects of variability in endogenous E2 levels on vascular function are important as spastic disorders, such as migraine headaches (MacGregor et al, 2006), Raynaud's phenomenon (Greenstein et al, 1996), and angina (Rosano et al, 1995), may be influenced by the menstrual cycle. Also, the greater incidence, yet less severity, of pulmonary hypertension in females suggest a complex interaction of E2 and ERs in the pulmonary circulation (Christou and Khalil, 2010).…”

Section: Discussionmentioning

confidence: 99%

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca2+]i in Mesenteric Microvessels of Female Rat

Mazzuca

Mata

et al. 2015

The Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

Estrogen interacts with estrogen receptors (ERs) to induce vasodilation, but the ER subtype and post-ER relaxation pathways are unclear. We tested if ER subtypes mediate distinct vasodilator and intracellular free Ca 21 concentration ([Ca 21 ] i ) responses via specific relaxation pathways in the endothelium and vascular smooth muscle (VSM). Pressurized mesenteric microvessels from female Sprague-Dawley rats were loaded with fura-2, and the changes in diameter and [Ca 21 ] i in response to 17b-estradiol (E2) (all ERs), PPT (4,49,-pyrazole-1,3,5-triyl]-tris-phenol) (ERa), diarylpropionitrile (DPN) (ERb), and G1 [(6)-1-[(3aR*,4S*,9bS*)-4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-tetrahydro:3H-cyclopenta(c)quinolin-8-yl]-ethanon] (GPR30) were measured. In microvessels preconstricted with phenylephrine, ER agonists caused relaxation and decrease in [Ca 21 ] i that were with E2 5 PPT . DPN . G1, suggesting that E2-induced vasodilation involves ERa . ERb . GPR30. Acetylcholine caused vasodilation and decreased [Ca 21 ] i , which were abolished by endothelium removal or treatment with the nitric oxide synthase blocker N v -nitro-L-arginine methyl ester (L-NAME) and the K 1 channel blockers tetraethylammonium (nonspecific)

show abstract

The Menstrual Cycle and Raynaud's Phenomenon

Cited by 33 publications

References 17 publications

Endogenous Estrogens Increase Postischemic Hyperemia in the Skin Microcirculation

Endogenous Estrogens Increase Postischemic Hyperemia in the Skin Microcirculation

17β-Estradiol mediates superior adaptation of right ventricular function to acute strenuous exercise in female rats with severe pulmonary hypertension

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca2+]i in Mesenteric Microvessels of Female Rat

Contact Info

Product

Resources

About