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Original Articles

Sympathetic neural control of the kidney in hypertension.

G F DiBona
https://doi.org/10.1161/01.HYP.19.1_Suppl.I28
Hypertension. 1992;19:I28
Originally published January 1, 1992
G F DiBona
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Abstract

Efferent renal sympathetic nerve activity is elevated in human essential hypertension as well as in several forms of experimental hypertension in animals. In addition, bilateral complete renal denervation delays the development and/or attenuates the magnitude of the hypertension in several different forms of experimental hypertension in animals. Efferent renal sympathetic nerve activity is known to have dose-dependent effects on renal blood flow, the glomerular filtration rate, renal tubular sodium and water reabsorption, and the renin secretion rate, which are capable of contributing, singly or in combination, to the development, maintenance, and exacerbation of the hypertensive state. Of the many factors known to influence the central nervous system integrative regulation of efferent renal sympathetic nerve activity, two environmental factors, a high dietary sodium intake and environmental stress, are capable of significant interaction. This resultant increase in efferent renal sympathetic nerve activity and subsequent renal functional alterations can participate in the hypertensive process. This is especially evident in the presence of an underlying genetic predisposition to the development of hypertension. Thus, interactions between environmental and genetic influences can produce alterations in the sympathetic neural control of renal function that play an important role in hypertension.

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Hypertension
January 1992, Volume 19, Issue 1 Suppl
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    Sympathetic neural control of the kidney in hypertension.
    G F DiBona
    Hypertension. 1992;19:I28, originally published January 1, 1992
    https://doi.org/10.1161/01.HYP.19.1_Suppl.I28

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    Sympathetic neural control of the kidney in hypertension.
    G F DiBona
    Hypertension. 1992;19:I28, originally published January 1, 1992
    https://doi.org/10.1161/01.HYP.19.1_Suppl.I28
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