109: Plasma endothelin-1, arterial stiffness, and mean arterial pressure in the first trimester are predictive of the diagnosis of preeclampsia

Preeclampsia (PE) is characterized by late pregnancy hypertension and proteinuria. PE causes significant morbidity for the maternal-fetal unit. Circulating endothelin-1 (ET-1), a potent vasoconstrictor, is elevated at the time of diagnosis of human PE. In addition, women with PE demonstrate arterial stiffness as early as the end of the first trimester. However, it is unknown if arterial stiffness is associated with a first trimester elevation in ET-1 and post-delivery placental ET-1. We hypothesized that 1) first trimester plasma ET-1 is elevated and is associated with arterial stiffness in women who develop PE; 2) first trimester ET-1 is predictive of PE; and 3) placental ET-1 is increased in PE. To address these questions, we performed a nested case-control study in women at risk for PE. First trimester plasma ET-1 was measured via ELISA; aortic stiffness and carotid beta-stiffness (CβS) were measured by carotid-femoral pulse-wave velocity (CFPWV) and carotid tonometry/ultrasound, respectively. While the maternal age of controls (n=126; age 30 ± 0.45 years) and PE (n=15; age 31 ± 1.3 years) were similar, the PE group had a higher first trimester BMI (35 ± 3 vs. 29 ± 1 kg/m 2 , p = 0.01), systolic (125 ± 2 vs. 113 ± 1 mmHg, p< 0.01) and diastolic blood pressure (68 ± 2 vs. 60 ± 1 mmHg, p< 0.01) compared with controls. In addition, first trimester plasma ET-1 (2.7 ± 0.4 vs. 2.0 ± 0.2 pg/mL, p < 0.01), CFPWV (7.2 ± 0.5 vs. 6.1 ± 0.2 m/s, p = 0.016), and CβS (8.4 ± 1.9 vs. 6.3 ± 0.3, p = 0.055) were higher in the PE group. Consistent with previous studies, third trimester plasma ET-1 was elevated in the PE group (2.9 ± 1.1 vs. 1.6 ± 0.1 pg/mL, p < 0.01) which paralleled a 2.5 fold increase in placental decidual ET-1 mRNA (p < 0.0001). ROC analyses showed that first trimester plasma ET-1 (AUC=0.71, p < 0.001) and CFPWV (AUC=0.70, p=0.014) were predictive of PE. This study supports the novel concept that elevated ET-1 in preeclampsia begins early in the first trimester and is associated with premature arterial stiffness. Further, these novel data suggest that ET-1 may play an important role in the first trimester prediction and pathogenesis of preeclampsia.

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Associations of Retinal Microvascular Diameters and Tortuosity With Blood Pressure and Arterial Stiffness

Hypertension ◽

10.1161/hypertensionaha.119.13752 ◽

2019 ◽

Vol 74 (6) ◽

pp. 1383-1390 ◽

Cited By ~ 6

Author(s):

Robyn J. Tapp ◽

Christopher G. Owen ◽

Sarah A. Barman ◽

Roshan A. Welikala ◽

Paul J. Foster ◽

...

Keyword(s):

Blood Pressure ◽

United Kingdom ◽

Mean Arterial Pressure ◽

Arterial Stiffness ◽

Arterial Pressure ◽

Retinal Vessel ◽

Vessel Diameter ◽

Automated Image Analysis ◽

Stiffness Index ◽

Arterial Stiffness Index

To examine the baseline associations of retinal vessel morphometry with blood pressure (BP) and arterial stiffness in United Kingdom Biobank. The United Kingdom Biobank included 68 550 participants aged 40 to 69 years who underwent nonmydriatic retinal imaging, BP, and arterial stiffness index assessment. A fully automated image analysis program (QUARTZ [Quantitative Analysis of Retinal Vessel Topology and Size]) provided measures of retinal vessel diameter and tortuosity. The associations between retinal vessel morphology and cardiovascular disease risk factors/outcomes were examined using multilevel linear regression to provide absolute differences in vessel diameter and percentage differences in tortuosity (allowing within person clustering), adjusted for age, sex, ethnicity, clinic, body mass index, smoking, and deprivation index. Greater arteriolar tortuosity was associated with higher systolic BP (relative increase, 1.2%; 95% CI, 0.9; 1.4% per 10 mmHg), higher mean arterial pressure, 1.3%; 0.9, 1.7% per 10 mmHg, and higher pulse pressure (PP, 1.8%; 1.4; 2.2% per 10 mmHg). Narrower arterioles were associated with higher systolic BP (−0.9 µm; −0.94, −0.87 µm per 10 mmHg), mean arterial pressure (−1.5 µm; −1.5, −1.5 µm per 10 mmHg), PP (−0.7 µm; −0.8, −0.7 µm per 10 mmHg), and arterial stiffness index (−0.12 µm; −0.14, −0.09 µm per ms/m 2 ). Associations were in the same direction but marginally weaker for venular tortuosity and diameter. This study assessing the retinal microvasculature at scale has shown clear associations between retinal vessel morphometry, BP, and arterial stiffness index. These observations further our understanding of the preclinical disease processes and interplay between microvascular and macrovascular disease.

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Impact of mean arterial pressure on progression of arterial stiffness in peritoneal dialysis patients under strict volume control strategy

Clinical Nephrology ◽

10.5414/cn107223 ◽

2012 ◽

Vol 77 (02) ◽

pp. 105-113 ◽

Cited By ~ 7

Author(s):

Mettem Sezis Demirci ◽

Ozkan Gungor ◽

Fatih Kircelli ◽

Juan Jesus Carrero ◽

Erhan Tatar ◽

...

Keyword(s):

Peritoneal Dialysis ◽

Mean Arterial Pressure ◽

Arterial Stiffness ◽

Arterial Pressure ◽

Control Strategy ◽

Volume Control ◽

Dialysis Patients

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First trimester elevation in circulating endothelin-1 and arterial stiffness are predictive of late pregnancy preeclampsia

Proceedings in Obstetrics and Gynecology ◽

10.17077/2154-4751.1431 ◽

2018 ◽

Vol 8 (3) ◽

pp. 1-2

Author(s):

Alexandria M. Betz ◽

Gary L. Pierce ◽

Donna A. Santillan ◽

Eric J Devor ◽

Sabrina M. Scroggins ◽

...

Keyword(s):

Arterial Stiffness ◽

Late Pregnancy ◽

First Trimester ◽

Endothelin 1

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Mean arterial pressure and arterial stiffness in Japanese population: a secondary analysis based on a cross-sectional study

Blood Pressure Monitoring ◽

10.1097/mbp.0000000000000471 ◽

2020 ◽

Vol 25 (6) ◽

pp. 310-317

Author(s):

Song Sheng

Keyword(s):

Mean Arterial Pressure ◽

Arterial Stiffness ◽

Arterial Pressure ◽

Japanese Population ◽

Secondary Analysis ◽

Cross Sectional Study ◽

Sectional Study ◽

Cross Sectional

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First Trimester Mean Arterial Pressure Measured Manually Versus Using an Automated Device and the Prediction of Preeclampsia: A Case-Cohort Study

Journal of Obstetrics and Gynaecology Canada ◽

10.1016/j.jogc.2019.06.017 ◽

2020 ◽

Vol 42 (3) ◽

pp. 277-283

Author(s):

Maxime Côté ◽

Amélie Boutin ◽

Cédric Gasse ◽

Suzanne Demers ◽

Emmanuel Bujold

Keyword(s):

Cohort Study ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

First Trimester

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Endothelin-1-induced vasoconstriction is inhibited during erection in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2001.281.2.r476 ◽

2001 ◽

Vol 281 (2) ◽

pp. R476-R483 ◽

Cited By ~ 16

Author(s):

T. M. Mills ◽

D. M. Pollock ◽

R. W. Lewis ◽

H. S. Branam ◽

C. J. Wingard

Keyword(s):

Nitric Oxide ◽

Smooth Muscle ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Muscle Relaxation ◽

Corpus Cavernosum ◽

Smooth Muscle Relaxation ◽

No Donor ◽

Intracavernosal Injection ◽

Endothelin 1

Recent evidence indicates that endothelin-1 (ET-1) might be a principal vasoconstrictor in the penis. We report that ET-1 injection into the cavernous sinuses before erection sharply reduced the magnitude of subsequent erections. Corpus cavernosum pressure-to-mean arterial pressure ratios (CCP/MAP), with maximal ganglionic stimulation, were 0.62 ± 0.05 before ET-1 injection and 0.31 ± 0.05 after, indicating that ET-1 acted as a vasoconstrictor. When ET-1 was injected during a maximal neurally induced erection, the ability of ET-1 to attenuate subsequent erections was diminished (CCP/MAP 0.75 ± 0.02 before ET-1, 0.61 ± 0.03 after). At submaximal stimulation voltages, injection of ET-1 during erection also attenuated its vasoconstrictive effect. Similarly, when ET-1 was injected during erection induced by intracavernosal injection of the nitric oxide (NO) donor NOR-1, subsequent erections were not significantly suppressed (CCP/MAP 0.53 ± 0.04 before ET-1, 0.45 ± 0.04 after). These findings that ET-1-induced vasoconstriction is attenuated during erection are consistent with the hypothesis that NO mediates erection both by initiating pathways that cause smooth muscle relaxation and by inhibiting the vasoconstrictive actions of ET-1.

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Migraine and Arterial Stiffness in the Brazilian Longitudinal Study of Adult Health: ELSA-Brasil

American Journal of Hypertension ◽

10.1093/ajh/hpaa005 ◽

2020 ◽

Vol 33 (5) ◽

pp. 458-464 ◽

Cited By ~ 1

Author(s):

Patricia Noemi Apelbaum ◽

Alessandra Carvalho Goulart ◽

Itamar de Souza Santos ◽

Paulo Andrade Lotufo ◽

Cristina Pellegrino Baena ◽

...

Keyword(s):

Longitudinal Study ◽

Mean Arterial Pressure ◽

Arterial Stiffness ◽

Arterial Pressure ◽

Pulse Wave Velocity ◽

Wave Velocity ◽

Sex Education ◽

Pulse Wave ◽

International Headache Society ◽

Adult Health

Abstract Background The mechanisms that underlie the link between migraine and cardiovascular diseases are not clear and arterial stiffness could play a role in that association. We analyzed the association between migraine and vascular stiffness measured by carotid-to-femoral pulse wave velocity (PWV-cf). Methods In a cross-sectional analysis of a well-defined population from the Longitudinal Study of Adult Health (ELSA-Brasil) with complete and validated information about migraine and aura according to the International Headache Society criteria, the association between arterial stiffness measured by PWV-cf was tested with multiple linear regression models [β (95% CI)] comparing migraine without aura (MO) and migraine with aura (MA) to the reference group no-migraine (NM). Subsequent adjustments were made for mean arterial pressure, age, sex, education level, physical activity, alcohol use, diabetes mellitus, smoking, antihypertensive medication, body mass index, waist circumference, triglycerides, and LDL-c level to test the independence of the association between migraine status and pulse wave velocity. Results We studied 4,649 participants, 2,521 women (25.7% MO and 15% MA) and 2,128 men (11% MO and 4.3% MA). In NM, MO, and MA standard PWV-cf were 8.67 (±1.71) 8.11 (±1.31) and 8.01 (±1.47) m/s, respectively. Unadjusted PWV-cf differed between NM, MA, and MO (P < 0.001). After adjustment for mean arterial pressure PWV-cf in NM did not differ anymore from MA (P = 0.525) and MO (P = 0.121), respectively. Fully adjusted models also yielded nonsignificant coefficients β (95% CI) −0.079 (−0.280; 0.122) and −0.162 (−0.391; 0.067) for MO and MA, respectively. Conclusion In this large cohort of middle-aged adults, aortic PWV was not associated with migraine.

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Coronary effects of endothelin-1 during acute hypertension in anaesthetized goats

Clinical Science ◽

10.1042/cs103s376s ◽

2002 ◽

Vol 103 (s2002) ◽

pp. 376S-379S ◽

Cited By ~ 1

Author(s):

Nuria FERNÁNDEZ ◽

María ANGELES MARTÍNEZ ◽

Angel Luis GARCÍA-VILLALÓN ◽

Luis MONGE ◽

Godofredo DIÉGUEZ

Keyword(s):

Mean Arterial Pressure ◽

Methyl Ester ◽

Arterial Pressure ◽

Coronary Flow ◽

Circumflex Coronary Artery ◽

Aortic Constriction ◽

Vascular Conductance ◽

Acute Hypertension ◽

Endothelin 1 ◽

Artery Flow

The coronary effects of endothelin-1 (ET-1) during acute hypertension were examined in anesthetized goats, where the left circumflex coronary artery flow was electromagnetically measured and hypertension was induced by constriction of the thoracic aorta. In six non-treated goats, aortic constriction increased arterial pressure (mean arterial pressure = 128±5mmHg) and coronary flow (by 34%) without changing coronary vascular conductance. In this case, ET-1 (0.01–0.3nmol) when injected intracoronarily, decreased coronary vascular conductance, which was similar in hypertension and in normotension. In eight NG-nitro-L-arginine methyl ester-treated goats, aortic constriction increased arterial pressure (mean arterial pressure = 131±5mmHg) and coronary flow (by 26%) and decreased coronary vascular conductance (by 17%). In this case, ET-1 (0.01–0.3nmol) also decreased coronary vascular conductance, which was similar in NG-nitro-L-arginine methyl ester-treated hypertension that observed in normotension. Therefore, acute hypertension attenuates the coronary vasoconstriction caused by ET-1, and this attenuation might be related to mechanisms other than changes in NO release.

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