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Titlebook: Endocrinology of the Vasculature; James R. Sowers Book 1996 Humana Press Inc. 1996 Diabetes.Diabetes mellitus.growth factor.insulin.signal

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Estrogen and Vascular Reactivity of myocardial infarction and stroke increases dramatically in women after the menopause . Of women ages 45-64 yr, one of nine have cardiovascular disease; yet after age 65, the ratio increases to one of three . Loss of endogenous estrogens associated with menopause contributes to the increased card
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C-Type Natriuretic Peptide, vasodilatory, and antimitogenic properties through actions of particulate.guanylyl cyclase and the second messenger guanosine 3’,5’-monophosphate (cGMP).. Brain natriuretic peptide (BNP) shares similar biological actions with ANP, is structurally similar (but genetically distinct), and functions v
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Vascular Actions of Insulin in Health and Diseaselar resistance. In this chapter, the physiologic role of insulin-induced skeletal muscle vasodilation and its mechanism including the interaction between insulin and the endothelium to modulate the endothelium-derived nitric oxide (NO) system are reviewed. Finally, the effect of insulin resistance o
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Angiotensin-Nitric Oxideular antagonists. The concept that the regulation of blood pressure (and vascular resistance) is the result of a balance between vasoconstriction and vasodilation may be somewhat oversimplified; nevertheless it is a natural place to begin to understand the intricate interaction between these two imp
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Altered Endothelial Function in Diabetes MellitusEarly observations suggested that endothelial injury may be a very early stage in diabetic micro-and macroangiopathy, and subsequent data support this view. A complete review of this rapidly expanding literature is beyond the scope of this chapter; the reader is referred to previous reviews .,. Our
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Effects of Hyperglycemia on Vascular Endothelium Nitric Oxide Metabolism effects, but vascular endothelial dysfunction appears to play an extremely important role. Accumulating data suggests that exposure to increased concentrations of glucose leads to endothelial dysfunction. Studies in diabetes have demonstrated elevations in plasma von Willebrand’s factor (1), dimini
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Evidence Linking Fatty Fat Acids, the Risk Factor Cluster, and Vascular Pathophysiologyew of the cluster and the possible pathogenetic link to the defect of insulin-mediated glucose disposal. Selected controversies in the insulin resistance—hypertension theory are addressed and another defect of insulin action, namely suppression of lipolysis and plasma NEFAs, is offered as an alterna
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