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Impact of Endothelin on Vascular Function in Hypertensive Postmenopausal Women
Author(s) -
Kuczmarski Andrew,
Harbert Becca,
Nathaniel Sangeetha,
Shoemaker Leena,
Wenner Megan
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.04547
Subject(s) - medicine , blood pressure , endothelin receptor , vasodilation , endothelin 1 , endocrinology , sodium nitroprusside , cardiology , receptor , nitric oxide
Endothelin‐1 contributes to vascular dysfunction in hypertensive adults through the endothelin‐A receptor (ETAR). However, our laboratory has recently shown an important role for the ETB receptor (ETBR) in regulating vascular function in women. We tested the hypothesis that hypertension is associated with a decline in ETBR function in postmenopausal women (PMW), and that this decline can be attenuated by anti‐hypertensive medication. We recruited normotensive PMW (NT; n=9, age: 60±4 yrs, BMI: 25±5 kg/m 2 ), hypertensive PMW naïve to therapy (HT; n=8, age: 59±5 yrs, BMI: 26±2 kg/m 2 ), and medicated hypertensive PMW (MedHT; n=8, age: 63±6 yrs, BMI: 25±5 kg/m 2 ). Blood pressure (BP) readings were taken on more than 1 visit to confirm BP category. We measured cutaneous vasodilatory responses to local heating via laser Doppler flowmetry during microdialysis perfusions of lactated Ringer's (Control) and ETBR blockade (BQ‐788, 300nM). Cutaneous vascular conductance (CVC) was calculated during the plateau phase of local heating (42°C) and normalized to maximal vasodilation achieved by perfusion of sodium nitroprusside (28mM) and heating to 43°C. A two‐way ANOVA was performed to compare the impact of hypertensive status on vasodilatory responses to ETBR antagonists. Groups were well matched except for resting blood pressure. Systolic BP was lowest in NT compared to the HT and MedHT groups (NT:122±9, HT; 148±11, MedHT: 131±10 mmHg; P<0.02), but diastolic BP was similar between groups (NT: 68±5, HT: 76±7, MedHT: 73±8 mmHg, P=0.15). Plasma ET‐1 was lower in NT compared to HT (NT: 1.29±0.24, HT: 1.83±0.2, MedHT: 1.57±0.44 pg/mL; P=0.03). Microvascular vasodilation (control site) was similar between groups (NT: 90±7, HT: 86±13, MedHT: 89±7 %CVC max ; P=0.56). Furthermore, ETBR blockade did not alter vasodilatory responses to local heating (NT: 90±7, HT: 91±9, MedHT: 84±11 %CVC max , P=0.99). These preliminary data suggest that the ETBR does not contribute to vascular dysfunction in hypertensive PMW. Additional data are needed to understand the mechanisms contributing to hypertension in women.