ETB Receptor Function is Modulated by Estradiol in Young Women

Our laboratory has recently demonstrated that a loss of endothelin-B (ETB) receptor mediated dilation contributes to impaired vasodilatory function in postmenopausal women. It is unclear if these changes are due to aging, or alterations in ovarian hormones that occur after menopause. The purpose of this study was to test the hypothesis that in a low estradiol state, there is a loss of ETB mediated dilation, and that estradiol administration reverses these responses and mediates dilation. Methods: We tested 8 young women (YW: 24±2 years, 23±1 kg/m 2 , mean arterial BP 84±2mHg) and 6 postmenopausal women (PMW: 56±1 years, 24±1 kg/m 2 , mean arterial BP 94±2mHg). In YW, we suppressed endogenous ovarian hormone production with daily gonadotropin-releasing hormone antagonist (GnRHant; Ganirelix) administration for 10 days, adding estradiol (E2, 0.1 mg/day, Vivelle dot patch) on days 4-10. PMW were tested at baseline and after 1-week E2 administration (0.1 mg/day, Vivelle dot patch). We measured nitric-oxide mediated vasodilation in the cutaneous circulation during local heating (42°C) via laser Doppler flowmetry, followed by microdialysis perfusions of sodium nitroprusside (28mM) with local heating to 43°C to elicit maximal dilation. Cutaneous vascular conductance (CVC) was calculated as cutaneous blood flow/mean arterial blood pressure, and expressed as a percent of maximal dilation. Results: ETB receptor blockade increased vasodilation in YW during hormone suppression with GnRHant (control: 88±3 vs. BQ-788: 94±2 CVC %max, P <0.05). However, ETB receptor blockaded tended to reduce vaodilation during E2 administration (control: 88±3 vs. BQ-788: 82±2 CVC %max, P =0.12). In PMW, ETB receptor blockade had no significant effect on vasodilatory responses (control: 90±4 vs. BQ-788: 95±2 CVC %max, P =0.20). Similarly, ETB receptor blockade did not alter vasodilation after E2 administration (control: 88±7 vs. BQ-788: 88±4 CVC %max). Conclusions: These preliminary data suggest that suppression of endogenous ovarian hormone production alters ETB receptor responses in young women, which is partially mediated by E2. Additional data are needed to determine ETB receptor sensitivity to E2 after menopause.

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ETA and ETB receptor function in pancreatitis-associated microcirculatory failure, inflammation, and parenchymal injury

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00181.2002 ◽

2003 ◽

Vol 285 (1) ◽

pp. G145-G153 ◽

Cited By ~ 28

Author(s):

T. Plusczyk ◽

B. Witzel ◽

M. D. Menger ◽

M. Schilling

Keyword(s):

Receptor Antagonist ◽

Tissue Injury ◽

Sodium Taurocholate ◽

Selective Inhibition ◽

Capillary Density ◽

Receptor Function ◽

Promising Target ◽

Etb Receptor ◽

Significant Attenuation ◽

Parenchymal Injury

The role of endothelin (ET)A and ETB receptor function in experimental pancreatitis is still not fully understood. Using a rat model of sodium taurocholate-induced pancreatitis and intravital microscopy, we therefore studied whether selective inhibition of ETA receptor function or combined ETA and ETB receptor blockade affects the development of pancreatitis-associated microcirculatory failure, inflammation, and parenchymal injury. Pretreatment with 10 mg/kg body wt of a combined ETA/B receptor antagonist, which is thought to mediate a simultaneous inhibition of both receptors, did not attenuate the pancreatitis-induced microcirculatory failure, inflammatory response, and parenchymal tissue injury. In contrast, pretreatment with a low concentration of the combined ETA/B receptor antagonist (4 mg/kg body wt), which predominantly inhibits the ETA receptor, revealed an improvement of some microcirculatory disorders and a significant attenuation of leukocyte recruitment and tissue injury. Furthermore, pretreatment with a selective ETA receptor antagonist (1 μg/kg body wt) almost abolished pancreatitis-associated capillary constriction, restored functional capillary density, and, consequently, improved overall nutritive perfusion. Importantly, the maintenance of an appropriate microcirculation by selective ETA receptor inhibition was accompanied by a significant attenuation of the inflammation-associated leukocytic response and by a marked reduction of parenchymal injury. Thus our study indicates that pancreatitis-associated development of microcirculatory failure, inflammation, and parenchymal injury is caused by ETs coupling onto the ETA receptor, which therefore may represent a promising target for novel strategies in the treatment of pancreatitis.

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ETB receptor-mediated vasodilation is regulated by estradiol in young women

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00087.2021 ◽

2021 ◽

Vol 321 (3) ◽

pp. H592-H598

Author(s):

Leena N. Shoemaker ◽

Katherine M. Haigh ◽

Andrew V. Kuczmarski ◽

Shane J. McGinty ◽

Laura M. Welti ◽

...

Keyword(s):

Young Women ◽

Gnrh Antagonist ◽

Endogenous Hormone ◽

Etb Receptor ◽

Endothelin B

The endothelin-B (ETB) receptor mediates vasodilation in young women, an effect lost following menopause. It is unclear whether these alterations are due to aging or changes in estradiol (E2). During endogenous hormone suppression (GnRH antagonist), blockade of ETB receptors enhanced cutaneous microvascular vasodilation. However, during E2 administration, blockade of ETB receptors attenuated vasodilation, indicating that the ETB receptor mediates dilation in the presence of E2. In young women, ETB receptors mediate vasodilation in the presence of E2, an effect that is lost when E2 is suppressed.

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Severe Paradoxical Dysphonia in Two Young Women

American Journal of Speech-Language Pathology ◽

10.1044/1058-0360.0203.52 ◽

1993 ◽

Vol 2 (3) ◽

pp. 52-55 ◽

Cited By ~ 1

Author(s):

Michael Collins ◽

Robert McDonald ◽

Robert Stanley ◽

Timothy Donovan ◽

C. Frank Bonebrake

Keyword(s):

Young Women ◽

Theoretical Basis ◽

Therapeutic Regimen ◽

Instrumental Data ◽

Relationship Of ◽

The Relationship

This report describes an unusual and persistent dysphonia in two young women who had taken a therapeutic regimen of isotretinoin for intractable acne. We report perceptual and instrumental data for their dysphonia, and pose a theoretical basis for the relationship of dysphonia to this drug. We also provide recommendations for reducing the risk of acquiring a dysphonia during the course of treatment with isotretinoin.

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What Do We Want Them To Be When They Grow Up?

Perspectives on Hearing and Hearing Disorders in Childhood ◽

10.1044/hhdc20.1.27 ◽

2010 ◽

Vol 20 (1) ◽

pp. 27-31

Author(s):

Lyn Robertson

Keyword(s):

Hearing Loss ◽

Social Development ◽

Young Women ◽

Hearing Aids ◽

Test Scores ◽

Spoken Language ◽

Language Therapy ◽

Profound Hearing Loss ◽

Children With Hearing Loss ◽

Learning To Listen

Abstract Learning to listen and speak are well-established preludes for reading, writing, and succeeding in mainstream educational settings. Intangibles beyond the ubiquitous test scores that typically serve as markers for progress in children with hearing loss are embedded in descriptions of the educational and social development of four young women. All were diagnosed with severe-to-profound or profound hearing loss as toddlers, and all were fitted with hearing aids and given listening and spoken language therapy. Compiling stories across the life span provides insights into what we can be doing in the lives of young children with hearing loss.

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