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This review outlines the effects of renal denervation on hypertensive heart disease, particularly on left ventricular hypertrophy and diastolic function, and on atrial fibrillation. The sympathoinhibitory effect of renal denervation, an important potential mechanism of its beneficial effects on heart disease, is also discussed.
Post-translational modifications (PTMs), such as O-GlcNAcylation and phosphorylation, are related to MR overactivation in diabetes and metabolic syndrome. Aldosterone binding promotes the proteasomal degradation of MR. Under conditions of high glucose, O-GlcNAcylation, and PKCβ-mediated MR phosphorylation are increased. Salt loading and oxidative stress also increase MR phosphorylation through the EGER/ERK pathway. PTMs inhibit ubiquitin attachment to the MR and interfere with the receptor’s aldosterone-induced proteasomal degradation. Consequently, they increase the sensitivity of the MR to aldosterone and exacerbate aldosterone-associated complications.
The hope is that renal denervation will solve not only hypertension-related complications but also the various problems associated with antihypertensive drugs that have a negative impact on quality of life.
Global guidelines that recommended the daily dietary intake goal for sodium and potassium exhibit variations. These disparities are influenced by diverse factors, including cultural dietary habits, socioeconomic status, health priorities, and available scientific research. Each population should follow the recommendations of their region.