Placental and Fetal Hemodynamics After Labetalol or Pindolol in a Sheep Model of Increased Placental Vascular Resistance and Maternal Hypertension

Erkinaro, Tiina; Kavasmaa, Tomi; Ylikauma, Laura Anneli; Mäkikallio, Kaarin; Haapsamo, Mervi; Acharya, Ganesh; Ohtonen, Pasi; Alahuhta, Seppo; Räsänen, Juha

doi:10.1177/1933719109335068

Cited by 10 publications

(8 citation statements)

References 40 publications

(66 reference statements)

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“…33 These findings are consistent with both Doppler ultrasound studies, which showed that α-methyldopa does not affect uteroplacental or fetal hemodynamics 33,34 and a sheep model of maternal hypertension in which labetalol and pindolol (another nonselective β-blocker) compromised uteroplacental perfusion. 35 Beta-blockers also may affect urethral development by interfering with Leydig cell activity in the testis. Leydig cells begin production of testosterone by week 8 and influence sexual differentiation.…”

Section: Discussionmentioning

confidence: 99%

Maternal Hypertension, Medication Use, and Hypospadias in the National Birth Defects Prevention Study

Zutphen

Werler

Browne

et al. 2014

Obstetrics &Amp; Gynecology

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OBJECTIVE To investigate whether antihypertensive classes and specific medications in early pregnancy increase the risk of severe hypospadias and to assess prior associations detected for late-treated and untreated hypertension in the National Birth Defects Prevention Study. METHODS Using telephone interviews from mothers of 2,131 children with severe hypospadias and 5,129 nonmalformed male control children for 1997–2009 births in a population-based case–control study, we estimated adjusted odds ratios (ORs) and 95% confidence intervals (CIs) with multivariable logistic regression. We adjusted P values to account for multiple testing. RESULTS Forty-eight (2.3%) case and 70 (1.4%) control mothers reported early pregnancy antihypertensive treatment, 45 (2.1%) case and 31 (0.6%) control mothers reported late treatment, and 315 (14.8%) case and 394 (7.7%) control mothers reported untreated hypertension. Selective β-blockers, centrally acting agents, renin–angiotensin system-acting agents, diuretics, and specific medications, methyldopa and atenolol, were not associated with hypospadias. Nonselective β-blockers (adjusted OR 3.22, 95% CI 1.47–7.05) were associated with hypospadias; however, P values adjusted for multiple testing were not statistically significant. We confirmed prior findings for associations between hypospadias and untreated hypertension (adjusted OR 2.09, 95% CI 1.76–2.48) and late initiation of treatment (adjusted OR 3.98, 95% CI 2.41–6.55). The increased risks would translate to severe hypospadias prevalences of 11.5, 17.7, and 21.9 per 10,000 births for women with untreated hypertension, nonselective β-blocker use, and late initiation of treatment, respectively. CONCLUSION Our study suggests a relationship between hypospadias and the severity of hypertension.

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Section: Discussionmentioning

confidence: 99%

Maternal Hypertension, Medication Use, and Hypospadias in the National Birth Defects Prevention Study

Zutphen

Werler

Browne

et al. 2014

Obstetrics &Amp; Gynecology

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“…Increased sympathetic activation in the pregnant dam may alter several physiological parameters that might affect the fetus. For example, sympathetic activation may increase maternal heart rate and blood pressure, which in turn may influence the blood flow to the placenta ( Erkinaro et al., 2009 ). Furthermore, the uterus contains alpha-adrenergic receptors, and stimulation of these receptors has been shown to increase both uterine blood flow and uterine contractility ( Sato et al., 1996 ).…”

Section: Potential Mechanisms Underlying the Pns Phenotypementioning

confidence: 99%

Individual differences in the effects of prenatal stress exposure in rodents

Boersma

Tamashiro

2015

Neurobiology of Stress

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Exposure to prenatal stress alters the phenotype of the offspring in adulthood. When the prenatal and adult environments do not match, these alterations may induce pathology risk. There are, however, large individual differences in the effects of prenatal stress. While some individuals seem vulnerable, others appear to be relatively resistant to its effects. In this review we discuss potential mechanisms underlying these individual differences with a focus on animal models. Differences between rodent models selected for stress coping traits are discussed. In addition, the role of circulating factors, like glucocorticoids and cytokines, factors involved in brain development and influences of epigenetic and genetic factors in prenatal stress induced phenotype are covered.

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“…Alternatively, despite its ß1 cardio-selective nature 53 , bisoprolol could have a direct effect on the placental vasculature. This is supported by evidence of ß1 receptors 54 , 55 in placental vasculature and placental vasoconstriction seen following exposure to ß blockers in vitro 56 , 57 . The potential negative effect of antenatal ß blocker use on fetal growth has long been considered 51 , 58 – 61 .…”

Section: Discussionmentioning

confidence: 73%

Prevalence of pre-eclampsia and adverse pregnancy outcomes in women with pre-existing cardiomyopathy: a multi-centre retrospective cohort study

Ormesher

Vause

Higson

et al. 2023

Sci Rep

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Pre-eclampsia is associated with postnatal cardiac dysfunction; however, the nature of this relationship remains uncertain. This multicentre retrospective cohort study aimed to determine the prevalence of pre-eclampsia in women with pre-existing cardiac dysfunction (left ventricular ejection fraction < 55%) and explore the relationship between pregnancy outcome and pre-pregnancy cardiac phenotype. In this cohort of 282 pregnancies, pre-eclampsia prevalence was not significantly increased (4.6% [95% C.I 2.2–7.0%] vs. population prevalence of 4.6% [95% C.I. 2.7–8.2], p = 0.99); 12/13 women had concurrent obstetric/medical risk factors for pre-eclampsia. The prevalence of preterm pre-eclampsia (< 37 weeks) and fetal growth restriction (FGR) was increased (1.8% vs. 0.7%, p = 0.03; 15.2% vs. 5.5%, p < 0.001, respectively). Neither systolic nor diastolic function correlated with pregnancy outcome. Antenatal ß blockers (n = 116) were associated with lower birthweight Z score (adjusted difference − 0.31 [95% C.I. − 0.61 to − 0.01], p = 0.04). To conclude, this study demonstrated a modest increase in preterm pre-eclampsia and significant increase in FGR in women with pre-existing cardiac dysfunction. Our results do not necessarily support a causal relationship between cardiac dysfunction and pre-eclampsia, especially given the population’s background risk status. The mechanism underpinning the relationship between cardiac dysfunction and FGR merits further research but could be influenced by concomitant ß blocker use.

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Placental and Fetal Hemodynamics After Labetalol or Pindolol in a Sheep Model of Increased Placental Vascular Resistance and Maternal Hypertension

Cited by 10 publications

References 40 publications

Maternal Hypertension, Medication Use, and Hypospadias in the National Birth Defects Prevention Study

Maternal Hypertension, Medication Use, and Hypospadias in the National Birth Defects Prevention Study

Individual differences in the effects of prenatal stress exposure in rodents

Prevalence of pre-eclampsia and adverse pregnancy outcomes in women with pre-existing cardiomyopathy: a multi-centre retrospective cohort study

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