Neurohormonal overactivation plays an important role in pulmonary hypertension (PH). In this context, renal denervation, which aims to inhibit the neurohormonal systems, may be a promising adjunct therapy in PH. In this proof-of-concept study, we have demonstrated in 2 experimental models of PH that renal denervation delayed disease progression, reduced pulmonary vascular remodeling, lowered right ventricular afterload, and decreased right ventricular diastolic stiffness, most likely by suppression of the renin-angiotensin-aldosterone system.
Keywords: AT1, angiotensin II type 1; Ea, right ventricular afterload; Eed, right ventricular stiffness; Ees, right ventricular contractility; MCT, monocrotaline model; PH, pulmonary hypertension; RAAS, renin angiotensin-aldosterone system; RD, renal denervation; SNS, sympathetic nervous system; SuHx, sugen combined with hypoxia model; pulmonary hypertension; renin angiotensin system; right ventricular failure; sympathetic nervous system.