The aim was to describe endothelium-dependent reactions of system hemodynamics to the reduction in system blood circulation (cardiac output) by orthostatic positioning of anesthetized rats. Head rise at 15, 30 and 45 degrees and NO synthesis depression increased the hypotensive reaction to orthostasis by 32, 60 and 71%, respectively, as compared with values prior to the block. This allows the conclusion concerning the recruitment of an NO-dependent vasodilative mechanism in vascular control. It was shown that NO modulated the arterial system reactivity to orthostasis the magnitude of which depended on baseline blood pressure. This relationship was reverse in the event of intact NO-synthase and linear in the event of NO synthesis depression. These data point to the significance of NO secretion for as baseline BD values, so mechanisms of orthostasis-induced hypotension.
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