Why the study?
Does prolonged electrical activation of the carotid baroreflex reduce arterial pressure in experimental models of hypertension?
Does prolonged electrical activation of the carotid baroreflex reduce arterial pressure in experimental models of hypertension?
This review highlights that the long-term blood pressure-lowering effects of baroreflex activation are heavily dependent on renal sympathoinhibition and subsequent increases in renal excretory function.
Does not support clinical adoption of baroreflex activation; leaves open translation of renal-dependent mechanisms from experimental models to human hypertension.
Device-based therapy for resistant hypertension by electrical activation of the carotid baroreflex is currently undergoing active clinical investigation, and initial findings from clinical trials have been published. The purpose of this mini-review is to summarize the experimental studies that have provided a conceptual understanding of the mechanisms that account for the long-term lowering of arterial pressure with baroreflex activation. The well established mechanisms mediating the role of the baroreflex in short-term regulation of arterial pressure by rapid changes in peripheral resistance and cardiac function are often extended to long-term pressure control, and the more sluggish actions of the baroreflex on renal excretory function are often not taken into consideration. However, because clinical, experimental, and theoretical evidence indicates that the kidneys play a dominant role in long-term control of arterial pressure, this review focuses on the mechanisms that link baroreflex-mediated reductions in central sympathetic outflow with increases in renal excretory function that lead to sustained reductions in arterial pressure.
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Lohmeier et al. (2012) studied this question.
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