Myoendometrial versus placental uterine arteries: Structural, mechanical, and functional differences in late-pregnant rabbits

Cipolla, Marilyn J.; Binder, Nancy D.; Osol, George

doi:10.1016/s0002-9378(97)70464-2

Cited by 46 publications

(43 citation statements)

References 22 publications

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“…Myogenic tone – the intrinsic ability of smooth muscle to sustain constriction in response to intravascular pressure – is absent in uterine radial arteries from nonpregnant animals, yet appears in those same types of arteries in late pregnancy [15,16,17]. …”

Section: Introductionmentioning

confidence: 99%

Effects of Pregnancy, Hypertension and Nitric Oxide Inhibition on Rat Uterine Artery Myogenic Reactivity

2010

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Background/Aims: The purpose of this study was to examine the effects of hypertension and nitric oxide (NO) inhibition on myogenic tone in uterine arteries during pregnancy. Methods: Premyometrial radial uterine arteries from nonpregnant and late pregnant Sprague-Dawley rats were evaluated for myogenic reactivity from the following groups: control, hypertensive/NO-inhibited (L-NAME treatment) and normotensive/NO-inhibited (L-NAME plus hydralazine). Results: In both nonpregnant and pregnant animals, L-NAME treatment significantly elevated blood pressures, while the addition of hydralazine made the animals normotensive. In nonpregnant animals, little myogenic tone was seen in controls; tone increased significantly in the L-NAME group, and was attenuated in those treated with L-NAME plus hydralazine. In pregnant animals, controls developed significant tone; this was reduced in the L-NAME group, and returned to control levels in the L-NAME plus hydralazine group. Conclusions: Dimensional measurements showed that arteries from the pregnant hypertensive group did not undergo expansive remodeling, suggesting that tone development is related to phenotypic alterations in vascular smooth muscle and/or altered physical forces secondary to adaptive changes in arterial diameter. These differences implicate pregnancy-specific pathways in the development and inhibition of myogenic tone, and point to potentially opposing roles of NO and hypertension.

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Section: Introductionmentioning

confidence: 99%

Effects of Pregnancy, Hypertension and Nitric Oxide Inhibition on Rat Uterine Artery Myogenic Reactivity

2010

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“…These phenomena have been reviewed with special emphasis on pregnant sheep (Rosenfeld 2001). Several studies have shown that the uterine blood vessels enlarge in size via both hypertrophic and hyperplastic mechanisms (Osol & Cipolla 1993a, Cipolla & Osol 1994, Cipolla et al 2000 and that a major part of these changes takes place during the last week of gestation in rats (St-Louis et al 1997). Moreover, these important structural alterations are accompanied by functional modulations of vascular reactivity (Osol & Cipolla 1993b, D'Angelo & Osol 1994, Ni et al 1997, St-Louis et al 1997, 2001, Zwart et al 1998.…”

Section: Introductionmentioning

confidence: 99%

Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake

St‐Louis¹,

Sicotte²,

Beauséjour³

et al. 2006

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Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin -angiotensin -aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low-and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na 1 ) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 mm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 mmol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.

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“…Myogenic response has been found as either increased or decreased in uterine arteries of pregnant, compared with nonpregnant, rats, mice, and rabbits (5,42,51).…”

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confidence: 99%

Pregnancy attenuates uterine artery pressure-dependent vascular tone: role of PKC/ERK pathway

Xiao

Buchholz²,

Zhang³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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]i was significantly greater for pressure-induced contraction of NPUA than that of PUA. Inhibition of PKC by calphostin C significantly attenuated the pressure-induced vascular tone and eliminated the difference of myogenic responses between NPUA and PUA. In contrast, the MAPKK (MEK) inhibitor PD-098059 had no effect on NPUA but significantly enhanced myogenic responses of PUA. In the presence of PD-098059, there was no difference in pressure-induced myogenic responses between NPUA and PUA. The results suggest that pregnancy downregulates pressure-dependent myogenic tone of the uterine artery, which is partly due to increased MEK/ERK activity and decreased PKC signal pathway leading to a decrease in Ca 2ϩ sensitivity of myogenic mechanism in the uterine artery during pregnancy.sheep; protein kinase C; extracellular signal-regulated kinase PREGNANCY IS ASSOCIATED WITH a significant increase in uterine blood flow that optimizes the delivery of oxygen and substrates to the developing fetus via the placenta. The adaptations in the uterine circulation to pregnancy are complex and are mediated in part by enhanced vasodilation and vascular remodeling. Previous studies (3,47,54,57) have focused on the endothelial adaptation and have shown an increase in endothelial nitric oxide synthesis/release in the uterine artery during pregnancy. The adaptation of smooth muscle contractile mechanisms is less clear. Pressure-dependent myogenic contraction is an important physiological mechanism that regulates basal vascular tone and is a significant contributor to the modulation of blood flow (6, 21). Myogenic response has been found as either increased or decreased in uterine arteries of pregnant, compared with nonpregnant, rats, mice, and rabbits (5, 42, 51).Although arterial myogenic behavior has been studied intensively for decades, the mechanisms by which vascular smooth muscle cells respond to changes in intraluminal pressure are still not fully understood. Previous studies (17,29,37) indicated that myogenic tone was highly dependent on an elevation of intracellular free Ca 2ϩ concentration ([Ca 2ϩ ] i ). However, it has also been demonstrated that Ca 2ϩ sensitization mechanisms contribute to myogenic tone (28,30,49,50). Activation of various kinase cascades regulating Ca 2ϩ sensitivity of the contractile apparatus may modulate the level of arteriolar myogenic reactivity (8, 21). PKC has been proposed to play an important role in the regulation of basal vascular tone and arterial caliber, the major determinants of blood flow (6, 41, 44). Pressure-induced activation of PKC has been proposed to induce myogenic tone without additional increases in Ca 2ϩ concentrations or myosin light chain (MLC 20 ) phosphorylation (18, 31). Our recent studies have also demonstrated in ovine uterine arteries that activation of PKC causes sustained contractions in the absence of changes in [Ca 2ϩ ] i and MLC 20 phosphorylation levels (56) and that the PKC-mediated contraction is significantly attenuated in the uterine artery during pregnancy (...

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Myoendometrial versus placental uterine arteries: Structural, mechanical, and functional differences in late-pregnant rabbits

Cited by 46 publications

References 22 publications

Effects of Pregnancy, Hypertension and Nitric Oxide Inhibition on Rat Uterine Artery Myogenic Reactivity

Effects of Pregnancy, Hypertension and Nitric Oxide Inhibition on Rat Uterine Artery Myogenic Reactivity

Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake

Pregnancy attenuates uterine artery pressure-dependent vascular tone: role of PKC/ERK pathway

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