Endothelin and neuropeptide Y are vasoconstrictors in human uterine blood vessels

Article Abstract:

Endothelin, a small protein that causes blood vessels to constrict, is released from the endothelial cells that line the inside of blood vessels. Because endothelin is present in blood vessels and can cause vasoconstriction, it may be involved in the development of vasospastic disorders, which are characterized by uncontrolled contraction of the blood vessels and hypertension (high blood pressure). Neuropeptide Y is another small protein that causes vasoconstriction; it is found in association with noradrenaline. Neuropeptide Y and noradrenaline are found in the peripheral sympathetic nerves which stimulate certain blood vessels, including those supplying the uterus and ovaries; the oviduct, a tube-like passage between the ovary and uterus; and the myometrium, the muscle layer of the uterus. The myometrial levels of noradrenaline and neuropeptide Y are higher in pregnant women with preeclampsia than in pregnant women without such complications. The blood flow to the uterus is controlled by various factors, including endothelial cell factors and nerves that stimulate the blood vessels. The effects of the vasoconstrictors endothelin and neuropeptide Y on the blood vessels supplying the uterus were assessed in segments of human uterine arteries and veins. A dose of 10 nanomoles per liter of endothelin produced a slow, long-lasting contraction of the blood vessels, whereas an equivalent doses of noradrenaline had no effect. Neuropeptide Y had no effect on the uterine artery, but increased muscle tone in the uterine vein and caused contraction at higher doses. A dose of 0.1 micromoles per liter of neuropeptide Y enhanced the contraction caused by one micromole per liter of noradrenaline, and the contraction caused by nerve stimulation. These findings suggest that endothelin and neuropeptide Y can regulate circulation in the uterus. (Consumer Summary produced by Reliance Medical Information, Inc.)

Vascular endothelium, Neuropeptide Y, Uterine circulation

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Inducible platelet adherence to human umbilical vein endothelium by anticardiolipin antibody-positive sera

Article Abstract:

A substance known as platelet-activating factor (PAF) may cause blood platelets to coagulate in the presence of anticardiolipin antibodies (ACA) in the blood. Blood platelet coagulation can block blood vessels, which can lead to stroke, miscarriage, slow fetal growth, and fetal death. Researchers found that ACA-positive blood samples had abnormally high coagulation, and that PAF regulated this abnormal coagulation. PAF did not cause increases in platelet coagulation in ACA-negative blood. Low doses of aspirin were found to inhibit the effect of PAF in ACA-positive blood. This finding may justify the use of low doses of aspirin to prevent platelet coagulation in individuals with circulating ACA in their blood.

Blood platelets, Cell aggregation, Anticardiolipin antibodies, Platelet activating factor

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Endothelin receptor A antagonism prevents hypoxia-induced intrauterine growth restriction in the rat

Article Abstract:

Endothelin may be an important contributor to intrauterine growth restriction (IUGR) due to oxygen deprivation, and treatment with an endothelin antagonist may prevent hypoxia-related IUGR. Researchers induced hypoxia in pregnant rats to analyze the effect of an endothelin receptor antagonist on IUGR. Rats receiving the endothelin antagonist produced heavier pups than rats not treated with the endothelin antagonist. Endothelin antagonist-treated rat pups had similar weights to rat pups from an environment with normal oxygenation.

Complications and side effects, Fetus, Fetal growth retardation, Fetal anoxia

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