61 research outputs found

    Endothelium-dependent responses and their potential relevance to the distribution of blood flow during hemorrhagic shock

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    The endothelium releases vasoactive substances in response to several circulating hormones and to changes in shear stress of the flowing blood across the endothelial surface. Because the distribution of receptors mediating the release of endothelium-derived factors is not uniform along the vascular bed, the vascular endothelium has a potential role in regulating regional blood flow and maintaining peripheral resistance during the course and recovery from hemorrhagic shock.link_to_subscribed_fulltex

    Endothelium-dependent responses and their potential relevance to the distribution of blood flow during hemorrhagic shock

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    The endothelium releases vasoactive substances in response to several circulating hormones and to changes in shear stress of the flowing blood across the endothelial surface. Because the distribution of receptors mediating the release of endothelium-derived factors is not uniform along the vascular bed, the vascular endothelium has a potential role in regulating regional blood flow and maintaining peripheral resistance during the course and recovery from hemorrhagic shock.link_to_subscribed_fulltex

    Progesterone and modulation of endothelium-dependent responses in canine coronary arteries

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    Chronic treatment with estrogens enhances some endothelium-dependent relaxations. Whether or not progesterone would exert a similar effect is unknown. Experiments were designed to determine the effect of chronic treatment with progesterone on endothelium-dependent responses. Adult female dogs were ovariectomized and pellets containing carrier substance, estrogen, progesterone, or estrogen plus progesterone were implanted subcutaneously. After 14-21 days coronary arteries were removed, cut into rings, and suspended for the measurement of isometric force in organ chambers in the presence of indomethacin. Endothelium-dependent relaxations to ADP, bradykinin, or the calcium ionophore did not differ among groups. However, relaxations to acetylcholine and to the α2-adrenergic agonist BHT-920 were greater in the estrogen-treated group than in the estrogen plus progesterone-treated group. In rings without endothelium, relaxations to nitric oxide and isoproterenol did not differ among groups. However, relaxations of the smooth muscle to ADP were greater in the progesterone-treated group than in the progesterone plus estrogen group. These results suggest that progesterone alone minimally affects endothelium-dependent responses. However, progesterone seems to antagonize the stimulatory effects of estrogen on two endothelium-dependent responses that are associated with pertussis toxin-sensitive guanine nucleotide regulatory proteins and the production of nitric oxide. These studies suggest that a specific receptor/second messenger system can be modulated by female reproductive steroid hormones.link_to_subscribed_fulltex

    Endothelium-dependent responses in isolated blood vessels of lower vertebrates

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    Is nitric oxide the only endothelium-derived relaxing factor in canine femoral veins?

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    Nitric oxide may be an endothelium-derived relaxing factor in systemic arteries and pulmonary veins. The endothelium-derived relaxing factor of systemic veins has not been characterized. Experiments were designed to determine whether the endothelium-derived relaxing factor of systemic veins shared chemical properties and mechanisms of action with nitric oxide. Rings of the canine femoral vein with and without endothelium were suspended in organ chambers for the measurement of isometric force. In rings without endothelium, relaxations to nitric oxide were augmented by superoxide dismutase plus catalase and were inhibited by hemoglobin, methylene blue, and LY 83583. The endothelium-dependent relaxations to acetylcholine and A23187 were not augmented by superoxide dismutase plus catalase but were inhibited by hemoglobin and only moderately reduced by either methylene blue or LY 83583. Relaxations to sodium nitroprusside were not inhibited by methylene blue and LY 83583. Relaxations to sodium nitroprusside were inhibited by ouabain and K+-free solution; those to nitric oxide were not. These results indicate that although the endothelium-derived relaxing factor released from canine systemic veins shares some chemical properties with nitric oxide, the mechanism by which relaxations are induced by the two differ. A factor dissimilar to nitric oxide but acting like sodium nitroprusside may be released by the endothelium of canine systemic veins.link_to_subscribed_fulltex

    Alpha2-adrenoceptors and endothelium-derived relaxing factor

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    The endothelium can release potent vasodilator substances, in particular prostacyclin and endothelium-derived relaxing factor. The triggers for the release of endothelium-derived relaxing factor include increases in levels of shear stress, neurotransmitters, autacoids, platelet products, and hormones. The endothelium-dependent response to catecholamines involves stimulation of alpha2-adrenoceptors on the endothelial cells. Indeed, in a number of blood vessels, selective alpha2-adrenergic agonists cause endothelium-dependent relaxations. These are seen most typically in blood vessels with long-term exposure to high flows and high partial pressures of oxygen. In addition to the release of endothelium-derived relaxing factor, alpha2-adrenergic agonists can stimulate postjunctional (postsynaptic) alpha2-adrenoceptors on vascular smooth muscles. These receptors, which are more abundant in hypertensive blood vessels, activate the contractile process. However, the alpha2-adrenergic vasoconstrictors act as partial agonists (with a limited receptor reserve) and hence their vasoconstrictor response is very sensitive to functional antagonists such as endothelium-derived relaxing factor. Thus, the presence of endothelial cells can blunt the vasoconstrictor response to these substances not only because of an augmented release of endothelium-derived relaxing factor but also because the vasoconstriction that they induce is particularly susceptible to the inhibitory effect of the factor.link_to_subscribed_fulltex

    Role of the endothelium in modulating vascular adrenergic receptor actions.

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