Vascular Physiology of the Nonpregnant Uterus

GreissJr., Frank C.; Rose, James C.

doi:10.1007/978-1-4684-5589-2_5

Cited by 9 publications

(8 citation statements)

References 59 publications

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“…Thus, it is possible that the PTHRP may play a role in controlling the rhythmicity and/or force of myometrial contraction in the antepartum period. Since uterine contractions severely depress blood flow (50), another possibility is that the PTHRP might act to dilate uterine blood vessels and assure adequate blood flow to the fetus and uterus during the late stages of pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Intrauterine occupancy controls expression of the parathyroid hormone-related peptide gene in preterm rat myometrium.

Thiede

Daifotis

Weir

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

156

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The parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHRP) genes are members of a gene family. Whereas PTH is a classical peptide hormone, mounting evidence suggests that the PTHRP may have predominately local actions. We report here that the PTHRP gene is expressed in rat myometrium, with a major peak in PTHRP mRNA expression occurring in the 48 hr immediately preceding parturition. A similar peak in peptide content was found in tissue extracts by biological and immunological assays, but the PTHRP could not be detected in the peripheral circulation or in uterine vein plasma during late gestation. By in situ hybridization histochemistry, PTHRP mRNA was demonstrated in both the longitudinal and circular layers of smooth muscle but was absent in the endometrium. The rise in myometrial PTHRP mRNA in late gestation was dependent upon intrauterine occupancy; it was greatly reduced or absent in nongravid uterine horns. These findings indicate that the expression of the PTHRP gene in preterm myometrium is under the control of a local stimulus and suggest that the PTIHRP may play a paracrine or autocrine role in the uterus during the antepartum period, possibly involving myometrial contractility.The parathyroid hormone-related peptide (PTHRP) was initially isolated (1-4) and its cDNA cloned (5-8) from human and animal tumors associated with the syndrome of humoral hypercalcemia of malignancy. The PTHRP has sequence similarity to parathyroid hormone (PTH) at its N terminus, which appears to account for its PTH-like actions when it is secreted into the systemic circulation by malignant tumors (9). However, the deduced PTHRP product is larger than PTH and has a more complex structure, suggesting that it may be subject to one or several posttranslational processing steps (5-8). The precise secretory form of the PTHRP has not been established for any cell type.Chromosomal localization studies and the structures of the PTH and PTHRP genes indicate that they arose by duplication from a common ancestral chromosome (10-12). Following this duplication event, the two genes have clearly evolved separately. The human PTHRP gene has been found to have an organization that is considerably more complex than that of the PTH gene (10)(11)(12)(13)(14). In addition, whereas the PTH gene is expressed predominately if not exclusively in parathyroid cells (15), the PTHRP gene is widely expressed in both endocrine and nonendocrine tissues. These sites of expression include tissues as diverse as skin (6,16,17), lactating mammary tissue (8), the chicken oviduct shell gland (18), the endocrine pancreas (19), and regions of the central nervous system (20). The role(s) of the PTHRP in these various sites is unknown, but the available evidence suggests that the peptide may be acting locally. Unique PTHRP receptors have not yet been identified.We report here that the PTHRP gene is expressed in rat myometrium and that this expression peaks in the antepartum period. This peak in PTHRP gene expression is confined to gravid ute...

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Section: Discussionmentioning

confidence: 99%

Intrauterine occupancy controls expression of the parathyroid hormone-related peptide gene in preterm rat myometrium.

Thiede

Daifotis

Weir

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

156

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“…Nevertheless, estrogen and its derivatives have been shown to increase uterine blood flow. 24 Indeed, uterine blood flowincreases approximately lO-fold immediately prior to estrus in ewes, and this increase temporally follows the increase in estrogen titers. 25 Nuclei of vascular smooth muscle cells in the arteries of the uterus have been shown to express estrogen and progesterone receptors.P" Receptor immunoreactivity was not found in uterine capillaries, veins, the endothelium lining the arteries, nor in vasculature from nonreproductive tissues.…”

Section: Potential Regulators Ofangiogenesis In Thementioning

confidence: 97%

Angiogenesis in the Uterus: Potential Regulation and Relation to Tumor Angiogenesis

Torry¹,

Rongish²

1992

American J Rep Immunol

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Except under certain pathological conditions such as wound healing and solid tumor growth, angiogenesis is a relatively rare event in the adult. One exception, however, is the angiogenesis that occurs during the cyclical changes in the female reproductive tract. Many factors, chemical as well as mechanical, have been shown to be capable of promoting or inhibiting angiogenesis in vivo and in vitro. However, despite intense research efforts, the mechanisms involved in the regulation of angiogenesis in vivo are not fully understood. In this article we briefly review the basic steps involved in angiogenesis and present examples of factors and conditions that may serve as potential regulators of angiogenesis in the nonpregnant uterus. Finally, we discuss some of the architectural, anatomical, and physiological differences between the microcirculatory beds established during normal, self-limited vessel growth and that associated with the uncontrolled, pathological vascular growth that accompanies tumor growth and metastasis.

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“…This suggests that elevated levels of endogenous estrogen are not required to maintain low impedance blood flow within the uteroplacental vascular bed during the second half of nonhuman primate pregnancy. uterus; fetus ESTROGEN HAS A WELL ESTABLISHED role in regulating several fundamentally important aspects of maternal cardiovascular physiology and uteroplacental blood flow dynamics (22,32,39,51,54). For example, the administration of estrogen to ovariectomized nonpregnant or pregnant sheep elevated uterine artery blood flow by regulating vasodilatatory mechanisms mediated by nitric oxide or other endothelium-derived mediators (10,20,26,33,35,52,53,56).…”

mentioning

confidence: 99%

Uterine and fetal blood flow indexes and fetal growth assessment after chronic estrogen suppression in the second half of baboon pregnancy

Aberdeen

Baschat²,

Harman³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Although estrogen regulates important aspects of maternal cardiovascular physiology, the role of estrogen on uteroplacental and fetal blood flow is incompletely understood. This study tested the hypothesis that chronically suppressing endogenous estrogen production during the second half of baboon pregnancy alters uterine and fetal blood flow dynamics assessed by ultrasonography. Pregnant baboons were untreated or treated daily with the aromatase inhibitor letrozole or letrozole plus estradiol on days 100-160 of gestation (term = 184 days). Blood flow dynamics were determined by Doppler ultrasonography on day 60 and longitudinally between days 110 and 160 of gestation. Letrozole decreased maternal serum estradiol and estrone concentrations by 95% (P < 0.001). Fetal growth biometrical parameters increased (P < 0.001) between days 110 and 160 of gestation and were similar in untreated and letrozole-treated animals. Uterine, umbilical, and fetal middle cerebral artery pulsatility index and resistance index declined (P < 0.01) by 30-50% and uterine artery volume flow increased sixfold (P < 0.001) between days 60 and 160, but values were similar in untreated, letrozole-treated, and letrozole plus estradiol-treated baboons. Thus uterine and fetal artery blood flow indexes, uterine artery volume flow, and fetal growth were maintained at normal levels despite chronic estrogen suppression in the second half of baboon pregnancy. This suggests that elevated levels of endogenous estrogen are not required to maintain low impedance blood flow within the uteroplacental vascular bed during the second half of nonhuman primate pregnancy.

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Vascular Physiology of the Nonpregnant Uterus

Cited by 9 publications

References 59 publications

Intrauterine occupancy controls expression of the parathyroid hormone-related peptide gene in preterm rat myometrium.

Intrauterine occupancy controls expression of the parathyroid hormone-related peptide gene in preterm rat myometrium.

Angiogenesis in the Uterus: Potential Regulation and Relation to Tumor Angiogenesis

Uterine and fetal blood flow indexes and fetal growth assessment after chronic estrogen suppression in the second half of baboon pregnancy

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