The contribution of renal sympathetic nerve activity to the development and progression of resistant hypertension, has been convincingly demonstrated in both preclinical and human experiments. Preclinical experiments in hypertension models of hypertension [5, 6, 14], have successfully used renal denervation as both an experimental tool and a therapeutic strategy, but even earlier, in the absence of appropriate drugs to pharmacologically reduce blood pressure in severely hypertensive patients, therapeutic splanchnicectomy and even radical surgical sympathectomy were used since the 1930s. These surgical techniques have been abandoned due to their severe side effects. Recent studies have further investigated the close relationship between kidneys and brain, and gave light to some important parameters of this transaction. Low frequency stimulation of the sympathetic system resulted in renin excretion only, intermediate frequency stimulation results on decreased urinary sodium excretion and high frequency stimulation, results on direct renal artery vasoconstriction, decrease in renal blood flow and decrease glomerular filtration rate [2, 5, 10].
CITATION STYLE
Toutouzas, K., Synetos, A., & Stefanadis, C. (2015). Vincristine local delivery for renal artery denervation. In Renal Denervation: A New Approach to Treatment of Resistant Hypertension (pp. 117–123). Springer-Verlag London Ltd. https://doi.org/10.1007/978-1-4471-5223-1_14
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