Roles of Ca++ and calmodulin in the PGI2 generation of cultured human vascular endothelial cells.

In pregnant women with severe diabetes mellitus, intrauterine growth retardation (IUGR) may occur despite hyperglycemia. Uterine blood flow may be an important factor in this process. Using pregnant streptozotocin‐induced diabetic rats (pregnant STZ‐diabetic rats), we evaluated functional and morphological changes in the endothelium, as well as platelet thromboxane A2 (TXA) production and their influence on uterine blood flow. Decreased basal endothelial prostacyclin (PGI2) production as well as significant attenuation of the production response to stimulus was noted, suggesting an impairment of PGI2 production. In the platelet, TXA2 production was augmented, leading to a hypercoagulable state. Decreased myometrial blood flow was documented. Scanning electron microscopy (SEM) revealed definite morphological abnormality of the endothelial cells, probably affecting the permeability to molecules, a major endothelial function. Based on these data, the endothelial derangements suggested by SEM and arachidonic acid metabolism alterations may affect fetal growth in the severe pregnant diabetic through alterations in uterine blood flow.

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Roles of Ca++ and calmodulin in the PGI2 generation of cultured human vascular endothelial cells.

Cited by 2 publications

References 7 publications

Calicum channel blockers and prostaglandin generation by gastric surface epithelial cells

Calicum channel blockers and prostaglandin generation by gastric surface epithelial cells

Vascular Wall Arachidonic Acid Metabolism and Fetal Growth in the Pregnant STZ‐Induced Diabetic Rat

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