Abstract
In genetically predisposed individuals, dietary salt loading causes the development or exacerbation of hypertension and increases sympathetic nervous system activity (OPARIL 1984). Approximately 50% of patients with essential hypertension are salt sensitive, i.e., they manifest a significant (>10%) increase in blood pressure in response to a high salt diet (Kawaskai et al. 1978; Fujita et al. 1980). Patients with salt sensitive essential hypertension have been shown to have inappropriately high plasma norepinephrine levels in relation to their urinary sodium excretion during periods of high salt intake (Campese et al. 1982). Thus, salt sensitive hypertensives fail to suppress plasma norepinephrine appropriately following ingestion of a highsalt diet. Further, they display significantly greater increments in plasma norepinephrine during upright posture than salt resistant hypertensives or normotensive control subjects (Campese et al. 1982).
This work has been supported in part by the National Heart, Lung, and Blood Institute Grants HL-22544, HL-36390, HL-35051, HL-39041, HL-37722, Grant-in-Aid from the American Heart Association, Alabama Affiliate, and by a Grant from the National Dairy Board and administered in cooperation with the National Dairy Council.
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Oparil, S. et al. (1989). The Neuronal Basis of Salt Sensitivity. In: Rettig, R., Ganten, D., Luft, F.C. (eds) Salt and Hypertension. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73917-0_8
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DOI: https://doi.org/10.1007/978-3-642-73917-0_8
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