Defining the differential sensitivity to norepinephrine and angiotensin II in the ovine uterine vasculature

Rosenfeld, Charles R.; DeSpain, Kevin; Liu, Xiao Tie

doi:10.1152/ajpregu.00424.2011

Cited by 8 publications

(7 citation statements)

References 57 publications

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“…As classic vasoconstrictors, AII and catecholamines play cardinal roles in the regulation of blood pressure [ 11 – 15 ]. In almost all peripheral blood vessels, norepinephrine is a major regulator to maintain basal vascular tension, and the norepinephrine-induced vasoconstriction is much more important than that by AII under physiological conditions [ 16 , 17 ].…”

Section: Discussionmentioning

confidence: 99%

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia

Gao

Tang

et al. 2017

Oncotarget

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The present study tested the hypothesis that angiotensin II plays a role in the regulation of placental vascular tone, which contributes to hypertension in preeclampsia. Functional and molecular assays were performed in large and micro placental and non-placental vessels from humans and animals. In human placental vessels, angiotensin II induced vasoconstrictions in 78.7% vessels in 155 tests, as referenced to KCl-induced contractions. In contrast, phenylephrine only produced contractions in 3.0% of 133 tests. In non-placental vessels, phenylephrine induced contractions in 76.0% of 67 tests, whereas angiotensin II failed to produce contractions in 75 tests. Similar results were obtained in animal placental and non-placental vessels. Compared with non-placental vessels, angiotensin II receptors and β -adrenoceptors were significantly increased in placental vessels. Compared to the vessels from normal pregnancy, angiotensin II-induced vasoconstrictions were significantly reduced in preeclamptic placentas, which was associated with a decrease in angiotensin II receptors. In addition, angiotensin II and angiotensin converting enzyme in the maternal-placenta circulation in preeclampsia were increased, whereas angiotensin I and angiotensin1-7 concentrations were unchanged. The study demonstrates a selective effect of angiotensin II in maintaining placental vessel tension, which may play an important role in development of hypertension in preeclampsia.

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Section: Discussionmentioning

confidence: 99%

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia

Gao

Tang

et al. 2017

Oncotarget

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“…The uterine vasculature is always refractory to ANG-II in women and sheep due to AT 2 R predominance in UA VSM throughout reproduction. 18,20 –22,43 In contrast, it is sensitive to α-adrenergic agonists and this increases in pregnancy 20,23,24,27,28,44 ; thus, infusion of α-adrenergic agents increases %▵UPVR more than simultaneous increases in %▵MAP and %▵UPBF falls. 13,19,45 This was seen at both gestational ages and was not due to differences in α 1 -AR expression in UA VSM during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…13,14 However, it is more sensitive to a-adrenergic stimulation and refractory to ANG-II compared to the systemic vasculature. 13,[15][16][17][18][19][20] The attenuated uterine responses to ANG-II are explained by predominant expression of type 2 ANG-II receptors (AT 2 Rs) in uterine VSM versus type 1 (AT 1 Rs) in peripheral VSM. [20][21][22][23] The explanation for the increased uteroplacental sensitivity to a-adrenergic agents is less clear but may include differences in a-adrenergic receptors, increases in VSM Ca 2þ sensitivity and contractile proteins, and/or remodeling.…”

Section: Introductionmentioning

confidence: 99%

“…13,[15][16][17][18][19][20] The attenuated uterine responses to ANG-II are explained by predominant expression of type 2 ANG-II receptors (AT 2 Rs) in uterine VSM versus type 1 (AT 1 Rs) in peripheral VSM. [20][21][22][23] The explanation for the increased uteroplacental sensitivity to a-adrenergic agents is less clear but may include differences in a-adrenergic receptors, increases in VSM Ca 2þ sensitivity and contractile proteins, and/or remodeling. [24][25][26][27][28] However, the mechanisms that contribute to the generalized uterine refractoriness to these agonists in pregnancy are unknown.…”

Section: Introductionmentioning

confidence: 99%

“…Potassium channels regulate vascular reactivity in numerous vascular beds. 20,29 Large conductance Ca 2þ -activated K þ channels (BK Ca ) are expressed in VSM, can modulate vasoconstrictor and vasodilator responses, and this function varies in different vascular beds. [29][30][31][32] The BK Ca consist of 4 a-subunits derived from a single gene product that form a homotetramer and undergo posttranslational modification, resulting in varied function.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Large Conductance Ca2+-Activated K+ Channels Modulate Uterine α1-Adrenergic Sensitivity in Ovine Pregnancy

Rosenfeld

Hynan²,

Liu

et al. 2014

Reprod. Sci.

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The uteroplacental vasculature is refractory to α-adrenergic stimulation, and large conductance Ca(2+)-activated K(+) channels (BK(Ca)) may contribute. We examined the effects of uterine artery (UA) BK(Ca) inhibition with tetraethylammonium (TEA) on hemodynamic responses to phenylephrine (PE) at 101 to 117 days and 135 to 147 days of ovine gestation, obtaining dose responses for mean arterial pressure (MAP), heart rate (HR), and uteroplacental blood flow (UPBF) and vascular resistance (UPVR) before and during UA TEA infusions. The UA α(1)-adrenergic receptors (α1-ARs) were assessed. The PE increased MAP and UPVR and decreased HR and UPBF dose dependently at both gestations (P < .001, analysis of variance). The %▵MAP was less at 135 to 147 days before and during TEA infusions (P ≤ .008); however, responses during TEA were greater (P ≤ .002). The PE increased %▵UPVR>>%▵MAP, thus %▵UPBF fell. The TEA enhanced PE-mediated increases in %▵UPVR at 135 to 147 days (P ≤ .03). The UA α(1)-AR expression was unchanged in pregnancy. Uterine vascular responses to PE exceed systemic vascular responses throughout pregnancy and are attenuated by BK(Ca) activation, suggesting BK(Ca) protect UPBF.

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Uterine Vascular Control Preconception and During Pregnancy

Fournier

D’Errico

Stapleton

2021

Comprehensive Physiology

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Successful pregnancy and reproduction are dependent on adequate uterine blood flow, placental perfusion, and vascular responsivity to fetal demands. The ability to support pregnancy centers on systemic adaptation and endometrial preparation through decidualization, embryonic implantation, trophoblast invasion, arterial/arteriolar reactivity, and vascular remodeling. These adaptations occur through responsiveness to endocrine signaling and local uteroplacental mediators. The purpose of this article is to highlight the current knowledge associated with vascular remodeling and responsivity during uterine preparation for and during pregnancy. We focus on maternal cardiovascular systemic and uterine modifications, endometrial decidualization, implantation and invasion, uterine and spiral artery remodeling, local uterine regulatory mechanisms, placentation, and pathological consequences of vascular dysfunction during pregnancy.

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Defining the differential sensitivity to norepinephrine and angiotensin II in the ovine uterine vasculature

Cited by 8 publications

References 57 publications

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia

Large Conductance Ca2+-Activated K+ Channels Modulate Uterine α1-Adrenergic Sensitivity in Ovine Pregnancy

Uterine Vascular Control Preconception and During Pregnancy

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