Abstract
Following volume expansion, the plasma acquires the capacity to cause natriuresis, inhibit membrane sodium transport, and increase vascular reactivity. The discovery of the atrial natriuretic factor (ANF) in 1981 provided a partial explanation for the first of these phenomena, but it was rapidly recognized that ANF was not an inhibitor of sodium transport,1 nor was it able to increase vascular reactivity.2 Thus it became apparent that a 20-year effort to identify a plasma-borne substance that was natriuretic by virtue of its ability to inhibit cellular sodium transport and which might increase vascular reactivity as a result of a similar action on vascular smooth muscle had not yet succeeded. Ten years later, in 1991, this effort appeared to have achieved its first major breakthrough.
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Doris, P.A. (1994). Endogenous Regulation of Sodium Pump Activity. In: Foà, P.P., Walsh, M.F. (eds) Ion Channels and Ion Pumps. Endocrinology and Metabolism, vol 6. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2596-6_12
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