The kallikrein-kinin system, but not vascular endothelial growth factor, plays a role in the increased vascular permeability associated with ovarian hyperstimulation syndrome

Kobayashi, Hiroshi; Okada, Yasukazu; Asahina, Takayuki; Gotoh, Jiro; Terao, T.

doi:10.1677/jme.0.0200363

Cited by 41 publications

(17 citation statements)

References 27 publications

(32 reference statements)

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“…The role of the inducible B1 receptor can be excluded, because of the short duration of the present experiments. The fi ndings are in agreement with the ascites-inducing role of kallikrein in the ovarian hyperstimulation syndrome [6].…”

Section: Discussionsupporting

confidence: 85%

Contribution of the Kallikrein/Kinin System to the Mediation of ConA-Induced Inflammatory Ascites

Baintner

2016

Acta Microbiologica et Immunologica Hungarica

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Intraperitoneal administration of concanavalin A (ConA, 25 mg/kg b.w.), a cell-binding plant lectin was used for inducing infl ammatory ascites, and potential inhibitors were tested in 1 h and 2.5 h experiments, i.e. still before the major infl ux of leucocytes. At the end of the experiment the peritoneal fl uid was collected and measured.The ConA-induced ascites was signifi cantly (p<0.01) and dose-dependently inhibited by icatibant (HOE-140), a synthetic polypeptide antagonist of bradykinin receptors. Aprotinin, a kallikrein inhibitor protein also had signifi cant (p<0.01), but less marked inhibitory effect. L-NAME, an inhibitor of NO synthesis, and atropine methylnitrate, an anticholinergic compound, were ineffective.It is concluded, that the kallikrein/kinin system contributes to the mediation of the ConA-induced ascites by increasing subperitoneal vascular permeability, independent of the eventual vasodilation produced by NO. It is known, that membrane glycoproteins are aggregated by the tetravalent ConA and the resulting distortion of membrane structure may explain the activation of the labile prekallikrein.Complete inhibition of the ConA-induced ascites could not be achieved by aprotinin or icatibant, which indicates the involvement of additional mediators.

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Section: Discussionsupporting

confidence: 85%

Contribution of the Kallikrein/Kinin System to the Mediation of ConA-Induced Inflammatory Ascites

Baintner

2016

Acta Microbiologica et Immunologica Hungarica

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“…49 However, other studies have cast doubt on the hypothesis that VEGF may be the causative factor in the vascular permeability associated with OHSS. 50 It is tempting to speculate that such discrepancies are because, at least in part, of the fact that although VEGF may be an important mediator in OHSS, it is by itself insufficient and the symptoms reflect the contribution of other factors, including EG-VEGF.…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of the Angiogenic Factor Genes Vascular Endothelial Growth Factor (VEGF) and Endocrine Gland-Derived VEGF in Normal and Polycystic Human Ovaries

Ferrara¹,

Frantz²,

LeCouter³

et al. 2003

The American Journal of Pathology

184

125

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Angiogenesis is a key aspect of the dynamic changes occurring during the normal ovarian cycle. Hyperplasia and hypervascularity of the ovarian theca interna and stroma are also prominent features of the polycystic ovary syndrome (PCOS), a leading cause of infertility. Compelling evidence indicated that vascular endothelial growth factor (VEGF) is a key mediator of the cyclical corpus luteum angiogenesis. However, the nature of the factor(s) that mediate angiogenesis in PCOS is less clearly understood. Endocrine glandderived (EG)-VEGF has been recently identified as an endothelial cell mitogen with selectivity for the endothelium of steroidogenic glands and is expressed in normal human ovaries. In the present study, we compared the expression of EG-VEGF and VEGF mRNA in a series of 13 human PCOS and 13 normal ovary specimens by in situ hybridization. EG-VEGF expression in normal ovaries is dynamic and generally complementary to VEGF expression in both follicles and corpora lutea. A particularly high expression of EG-VEGF was detected in the Leydig-like hilus cells found in the highly vascularized ovarian hilus. In PCOS ovaries, we found strong expression of EG-VEGF mRNA in theca interna and stroma in most of the specimens examined, thus spatially related to the new blood vessels. In contrast, VEGF mRNA expression was most consistently associated with the granulosa cell layer and sometimes the theca, but rarely with the stroma. Angiogenesis is a key aspect of normal cyclical ovarian function. Follicular growth and the development of the corpus luteum (CL) are dependent on the proliferation of new capillary vessels.

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“…The course of severe OHSS cannot be predicted by the overall pattern of circulating free VEGF [11]. The rise in vascular permeability induced by ascites in OHSS patients could not be blocked by the administration of anti-VEGF antibodies in an in vitro assay and an in vivo animal experiment [12]. These reports suggest that other factors including kinin-kallikrein system [13], renin-angiotensin system, prostaglandin, cytokines and nitric oxide must also be involved in the pathogenesis of OHSS.…”

mentioning

confidence: 89%

Organ-Specific Production Control of Vascular Endothelial Growth Factor in Ovarian Hyperstimulation Syndrome-Model Rats

et al. 2003

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Abstract. Overproduction of vascular endothelial growth factor (VEGF) following human chorionic gonadotropin (hCG) stimulation has been implicated as one of the causative factors in the development of ovarian hyperstimulation syndrome (OHSS). The objective of this study was to clarify the action of hCG and progesterone, one of the possible factors for OHSS, on VEGF production and gene expression using OHSS-model rats. A total of 40 immature female Wistar rats were stimulated with 10 IU of equine chorionic gonadotropin for four consecutive days from the 22nd to 25th day of life followed by subcutaneous injection of 30 IU of hCG on the 26th day of life. RU486 and progesterone were injected 24 h after the hCG injection. Tissues and blood samples were collected on the 28th day. hCG elicited VEGF production in the OHSS-model rat ovaries. Ovarian weights of the OHSS model rats were significantly increased through day 26 by the ovarian stimulation with single dose of 30 IU hCG. Addition of anti-progesterone RU486, which reduced the ovarian enlargement, attenuated VEGF production dose dependently whereas the VEGF gene expression was stable. In the lung and liver, neither hCG nor RU486 affected VEGF production and gene expression. These results suggested that progesterone regulates VEGF production at the post-transcriptional level in a tissue specific manner in the hyperstimulated ovary.

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The kallikrein-kinin system, but not vascular endothelial growth factor, plays a role in the increased vascular permeability associated with ovarian hyperstimulation syndrome

Cited by 41 publications

References 27 publications

Contribution of the Kallikrein/Kinin System to the Mediation of ConA-Induced Inflammatory Ascites

Contribution of the Kallikrein/Kinin System to the Mediation of ConA-Induced Inflammatory Ascites

Differential Expression of the Angiogenic Factor Genes Vascular Endothelial Growth Factor (VEGF) and Endocrine Gland-Derived VEGF in Normal and Polycystic Human Ovaries

Organ-Specific Production Control of Vascular Endothelial Growth Factor in Ovarian Hyperstimulation Syndrome-Model Rats

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