Abstract

With increasing evidence that the sympathetic nervous system plays a critical role in the development of hypertension, focus is turning to how these signals translate to a chronic increase in arterial pressure. The kidney's role in the control of salt and water homeostasis makes it an obvious target for such investigations. However, to date many studies have been restricted to experiments that last only a few hours, or at most, a few days, whereas others may use indirect methods of assessing sympathetic activity rather than direct recordings. We review current approaches used to determine the effects of renal sympathetic nerve activity (SNA) on arterial pressure and suggest possible avenues of future investigation. We propose that although afferent inputs, such those as from chemoreceptors and baroreceptors, are important for the short-term control of blood pressure via regulation of SNA to multiple organs, it is highly likely that alternative signals are important for setting the long-term level of renal SNA. Emerging evidence indicates that circulating angiotensin II is a hormone that may act on the central nervous system to regulate renal SNA, renal function, and, therefore, blood pressure. Future studies on the genesis of hypertension should focus more on determining the mediators of long-term levels of renal SNA.

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