Adrenergic regulation of contractile activity in the smooth muscle of umbilical vessels

Orchakov, V. A.; Vladimirova, I. A.; Shuba, M. P.; Artamonov, V. S.

doi:10.1007/bf01052747

Cited by 2 publications

(2 citation statements)

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“…Endothelial factors, including nitric oxide, PGI2, H2S and EDHF, are well known to evoke vasorelaxation, whereas the production of ET-1, TXA2 or VSMC depolarization causes vasoconstriction [10]. Figure 4 summarizes the major mechanisms initiated by the activation of adrenergic receptors in the endothelium and in the VSMC layer of resistance-size vessels in animal models, and in the human fetoplacental vasculature [94–131].…”

Section: Methodsmentioning

confidence: 99%

Fetoplacental vascular effects of maternal adrenergic antihypertensive and cardioprotective medications in pregnancy

Tropea,

Mavichak,

Evangelinos

et al. 2023

Journal of Hypertension

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Maternal cardiovascular diseases, including hypertension and cardiac conditions, are associated with poor fetal outcomes. A range of adrenergic antihypertensive and cardioprotective medications are often prescribed to pregnant women to reduce major maternal complications during pregnancy. Although these treatments are not considered teratogenic, they may have detrimental effects on fetal growth and development, as they cross the fetoplacental barrier, and may contribute to placental vascular dysregulation. Medication risk assessment sheets do not include specific advice to clinicians and women regarding the safety of these therapies for use in pregnancy and the potential off-target effects of adrenergic medications on fetal growth have not been rigorously conducted. Little is known of their effects on the fetoplacental vasculature. There is also a dearth of knowledge on adrenergic receptor activation and signalling within the endothelium and vascular smooth muscle cells of the human placenta, a vital organ in the maintenance of adequate blood flow to satisfy fetal growth and development. The fetoplacental circulation, absent of sympathetic innervation, and unique in its reliance on endocrine, paracrine and autocrine influence in the regulation of vascular tone, appears vulnerable to dysregulation by adrenergic antihypertensive and cardioprotective medications compared with the adult peripheral circulation. This semi-systematic review focuses on fetoplacental vascular expression of adrenergic receptors, associated cell signalling mechanisms and predictive consequences of receptor activation/deactivation by antihypertensive and cardioprotective medications.

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Section: Methodsmentioning

confidence: 99%

Fetoplacental vascular effects of maternal adrenergic antihypertensive and cardioprotective medications in pregnancy

Tropea,

Mavichak,

Evangelinos

et al. 2023

Journal of Hypertension

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“…CGRP is known to increase noradrenergic and adrenergic sympathetic outflow after activation of various hypothalamic nuclei. [33][34][35] Thus, it is possible that constriction of the umbilical vascular bed after exogenous CGRP during NO blockade may be mediated via activation of adrenoreceptors in the umbilical vasculature; 36 an effect that clearly is overridden by the potent NO-dependent actions of the peptide in this essential vascular bed. Alternatively, constrictor actions of CGRP during NO blockade may be similar to those of acetylcholine in vessels once denuded of the endothelium or in intact vessels after NO synthase blockade, as elegantly demonstrated by Furchgott and Zawadzki 37 and Librizzi and colleagues.…”

Section: Thakor and Giussani Cgrp And Fetal Cardiovascular Regulationmentioning

confidence: 99%

Role of Nitric Oxide in Mediating In Vivo Vascular Responses to Calcitonin Gene-Related Peptide in Essential and Peripheral Circulations in the Fetus

Thakor

Giussani

2005

Circulation

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Background-The role of calcitonin gene-related peptide (CGRP) in cardiovascular regulation is gaining clinical and scientific interest. In the adult, in vivo studies have shown that CGRP-stimulated vasodilation in several vascular beds depends, at least in part, on nitric oxide (NO). However, whether CGRP acts as a vasodilator in the fetus in vivo and whether this effect is mediated via NO have been addressed only minimally. This study tested the hypothesis that CGRP has potent NO-dependent vasodilator actions in essential and peripheral vascular beds in the fetus in late gestation. Methods and Results-Under anesthesia, 5 fetal sheep at 0.8 gestation were instrumented with vascular catheters and Transonic flow probes around an umbilical artery and a femoral artery. Five days later, fetuses received 2-and 5-g doses of exogenous CGRP intra-arterially in randomized order. Doses were repeated during NO blockade with the NO clamp. This technique permits blockade of de novo synthesis of NO while compensating for tonic production of the gas, thereby maintaining basal cardiovascular function. CGRP resulted in potent and long-lasting NO-dependent dilation in the umbilical and femoral circulations, hypotension, and a positive cardiac chronotropic effect. During NO blockade, the femoral vasodilator response to CGRP was diminished. In contrast, in the umbilical vascular bed, the dilator response was not only prevented but reversed to vasoconstriction. Conclusions-CGRP

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Adrenergic regulation of contractile activity in the smooth muscle of umbilical vessels

Cited by 2 publications

References 1 publication

Fetoplacental vascular effects of maternal adrenergic antihypertensive and cardioprotective medications in pregnancy

Fetoplacental vascular effects of maternal adrenergic antihypertensive and cardioprotective medications in pregnancy

Role of Nitric Oxide in Mediating In Vivo Vascular Responses to Calcitonin Gene-Related Peptide in Essential and Peripheral Circulations in the Fetus

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