High Altitude Reduces NO-Dependent Myometrial Artery Vasodilator Response During Pregnancy
Autor: | HeaMi Yi, Colleen G. Julian, Ramón A. Lorca, Meghan Donnelly, Anna G. Euser, Sydney L. Lane, Elise S. Bales, Hisham Nsier, Lorna G. Moore |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Adult medicine.medical_specialty Endothelium Adolescent Bradykinin Vasodilation Blood Pressure 030204 cardiovascular system & hematology Muscle Smooth Vascular Article 03 medical and health sciences Thromboxane A2 chemistry.chemical_compound Young Adult 0302 clinical medicine Pre-Eclampsia Pregnancy Risk Factors Internal medicine Internal Medicine medicine Humans Phenylephrine Altitude Hypoxia (medical) Middle Aged Uterine Artery 030104 developmental biology medicine.anatomical_structure Endocrinology chemistry Female Sodium nitroprusside Endothelium Vascular medicine.symptom Nitric Oxide Synthase Acetylcholine medicine.drug |
Zdroj: | Hypertension |
ISSN: | 1524-4563 |
Popis: | The chronic hypoxia of high-altitude (HA) residence reduces uterine artery blood flow during pregnancy, likely contributing to an increased frequency of preeclampsia and intrauterine growth restriction. We hypothesized that this lesser pregnancy blood flow rise was due, in part, to reduced vasodilation of myometrial arteries (MAs). Here, we assessed MA vasoreactivity in healthy residents of high (2902±39 m) or low altitude (LA; 1669±10 m). MA contractile responses to potassium chloride, phenylephrine, or the thromboxane A2 agonist U46619 did not differ between LA and HA women. Acetylcholine vasodilated phenylephrine or U466119 preconstricted MAs at LA, yet had no effect on HA MAs. In contrast, another vasodilator, bradykinin, relaxed MAs from both altitudes similarly. At LA, the NO synthase inhibitor L-N G -nitroarginine methyl ester decreased both acetylcholine and bradykinin vasodilation by 56% and 33%, respectively. L-N G -nitroarginine methyl ester plus the COX (cyclooxygenase) inhibitor indomethacin had similar effects on acetylcholine and bradykinin vasodilation (68% and 42% reduction, respectively) as did removing the endothelium (78% and 50% decrease, respectively), suggesting a predominantly NO-dependent vasodilation at LA. However, at HA, L-N G -nitroarginine methyl ester did not change bradykinin vasodilation, whereas indomethacin or endothelium removal decreased it by 28% and 72%, respectively, indicating impaired NO signaling at HA. Suggesting that the impairment was downstream of eNOS (endothelial NO synthase), HA attenuated the vasodilation elicited by the NO donor sodium nitroprusside. We concluded that reduced NO-dependent MA vasodilation likely contributes to diminished uteroplacental perfusion in HA pregnancies. |
Databáze: | OpenAIRE |
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