Inhibition of oestrogen-induced increase in uterine blood flow in the rat

Phaily, S.; Senior, Judith

doi:10.1111/j.2042-7158.1978.tb13380.x

Cited by 5 publications

(4 citation statements)

References 7 publications

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“…Kinins have been implicated in estrogen-induced vasodilation [43] and in uterine blood flow regulation in established pregnancy [10]. Our findings of immunoreactive tissue kallikrein, kallikrein mRNA, and potent kininase activity, as well as the confirmation of kininogen [44] in uterine homogenates, demonstrate that all the components of the kallikrein-kinin system are present in the uterus, and support its local role.…”

Section: Discussionsupporting

confidence: 72%

Uterine Kallikrein in the Early Pregnant Rat1

Valdés

Corthorn

Scicli

et al. 1993

Biology of Reproduction

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Uterine homogenates of cycling and early pregnant Sprague Dawley rats and purified rat urinary kallikrein showed similar curves of displacement of 125I-kallikrein binding to a polyclonal antibody. Uterine kallikrein concentration measured by RIA was 8.7 +/- 2 SEM ng/g wet weight during the cycle (n = 6 in diestrus and metestrus) and 20.8 +/- 2 SEM (n = 7) ng/g wet weight on Day 7 of pregnancy (P7) (p < 0.001). On P7, kallikrein concentration was increased 12.4-fold in the implantation nodes, as compared to the interimplantation segments. Uterine homogenates of rats on P7, submitted to DEAE-cellulose chromatography and Sephadex gel filtration, yielded two fractions containing kallikrein immunoreactivity and kininogenase activity, with molecular masses that ranged from 120-125 kDa and 39-43 kDa, respectively. In the RIA, both fractions displayed parallelism with purified kallikrein. Enzymatic activity was expressed after activation by trypsin. It was inhibited by aprotinin, PMSF, p-amino-benzamidine, and leupeptin, but not by soybean or ovomucoid trypsin inhibitors. Kallikrein mRNA was demonstrated by reverse transcriptase/polymerase chain reaction in uteri of nonpregnant and P7 rats. These results show that rat uterus synthesizes one or more serine proteases that are immunologically and enzymatically related to tissue kallikrein in the implantation node on P7--determined both by an increment of whole uterus kallikrein content and a depletion of the interimplantation segments--suggests that kallikrein may play a role in the vasoactive changes of implantation.

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Section: Discussionsupporting

confidence: 72%

Uterine Kallikrein in the Early Pregnant Rat1

Valdés

Corthorn

Scicli

et al. 1993

Biology of Reproduction

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“…All these changes could be expressions of estrogen regulation, since the two extreme values coincide with the high and low levels of estrogen attained in ovarian vein and systemic circulation [15,16]. Further support for an association between estrogens and kallikrein is provided by the vasoactive effects of estrogens [17][18][19][20][21] and by the fact that estrogen-induced vasodilation can be diminished by interfering with the generation of kinins [22]. Progesterone levels during the cycle show a peak on the evening of proestrus and another during metestrus [23], and are thus not connected with those here reported for IR kallikrein.…”

Section: Discussionmentioning

confidence: 97%

Variations in Uterine Kallikrein during Cycle and Early Pregnancy in the Rat1

Corthorn

Valdés

1994

Biology of Reproduction

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We have previously demonstrated the presence of tissue kallikrein and its mRNA in rat uterus, and an increase of the immunoreactive enzyme on Day 7 of gestation, which suggests a hormonal regulation and a role in implantation. This study pursued the sequential variations during the cycle and early pregnancy. During the estrous cycle, immunoreactive uterine kallikrein levels showed a recurrent pattern, with the highest value on proestrus (12.9 +/- 1.5 ng/uterus or 0.49 +/- 0.03 ng/mg protein), and the lowest on metestrus (4.1 ng +/- 0.5 ng or 0.30 +/- 0.03 ng/mg protein); p < 0.05. During gestation, values on Day 1 (6.1 +/- 0.4 ng/uterus or 0.30 +/- 0.01 ng/mg protein) and Day 3 (4.9 +/- 0.3 ng or 0.35 +/- 0.01 ng/mg protein) were similar to levels during estrus and diestrus; a progressive rise, observed from Day 5 (8.2 +/- 1.1 ng or 0.43 +/- 0.02 ng/mg protein), attained the highest value on Day 7 (15.8 +/- 1.7 ng or 0.78 +/- 0.05 ng/mg protein); p < 0.05. The variations observed during the cycle and early gestation coincide with those described for ovarian steroids and uterine vasoactive changes, suggest the hormonal regulation of uterine kallikrein levels, and support its role in implantation.

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“…Tamoxifen inhibits prostaglandin synthesis in vitro (Fenwick, Jones, Naylor, Poyser & Wilson, 1977;Sharma & Pugh, 1977) but this is unlikely to be the mechanism by which this anti-oestrogen inhibits the uterine blood flow response to oestrogen because inhibition of prostaglandin synthesis alone only reduced the response by 50% (Phaily & Senior, 1978a). Inhibition of the action of prostaglandins, kinins and histamine was needed to abolish the oestrogen-induced uterine hyperaemia (Phaily & Senior, 1978b). Furthermore, nafoxidine, which is not known to be a prostaglandin synthesis inhibitor, also inhibited oestrogen-induced uterine blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…Oestrogens are known to produce an increase in uterine blood flow and volume as well as an increase in uterine weight (Spaziani & Suddick, 1967;Spaziani, 1975;Phaily & Senior, 1978a). Previous work has shown that oestrogen-induced uterine blood flow evoked during the first hour after treatment may be modified by substances which inhibit the synthesis or action of histamine, kinins and prostaglandins (Phaily & Senior, 1978b). The mechanism of action of oestrogen in inducing blood flow increases could be through the oestrogen receptors present in the uterus of the ovariectomized rat or by a direct effect on vascular smooth muscle.…”

Section: Introductionmentioning

confidence: 99%

Anti-oestrogen modification of uterine responses to oestrogen in the rat

Majid¹,

Senior²

1982

Reproduction

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Oestradiol (single injection) resulted in a peak in uterine blood flow 3 h later with a secondary rise in blood flow at 30 h. Uterine wet and dry weights increased more slowly and were still above control values 24 h after the injection. If a second injection of oestradiol was given 24 h after the first then uterine blood flow was again maximal at 3 h but remained at this level for a further 3 h, probably due to the secondary rise induced by the first injection. Uterine wet weight was further increased by the second injection of oestradiol but the effect did not occur until 6 h after the oestrogen treatment. Pretreatment with an anti-oestrogen, tamoxifen or nafoxidine, inhibited or reduced significantly the uterine weight and uterine blood flow responses to oestrogen but increased uterine weights and produced some increase in uterine blood flow when given alone. It is suggested that both blood flow and weight responses to oestrogen in the uterus are mediated through the oestrogen receptors.

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Inhibition of oestrogen-induced increase in uterine blood flow in the rat

Cited by 5 publications

References 7 publications

Uterine Kallikrein in the Early Pregnant Rat1

Uterine Kallikrein in the Early Pregnant Rat1

Variations in Uterine Kallikrein during Cycle and Early Pregnancy in the Rat1

Anti-oestrogen modification of uterine responses to oestrogen in the rat

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