Renal sympathetic nerve activation via α₂-adrenergic receptors in chronic kidney disease progression
Kidney Research and Clinical Practice
;
: 6-14, 2019.
Artículo
en Inglés
| WPRIM
| ID: wpr-758980
ABSTRACT
Chronic kidney disease (CKD) is increasing worldwide without an effective therapeutic strategy. Sympathetic nerve activation is implicated in CKD progression, as well as cardiovascular dysfunction. Renal denervation is beneficial for controlling blood pressure (BP) and improving renal function through reduction of sympathetic nerve activity in patients with resistant hypertension and CKD. Sympathetic neurotransmitter norepinephrine (NE) via adrenergic receptor (AR) signaling has been implicated in tissue homeostasis and various disease progressions, including CKD. Increased plasma NE level is a predictor of survival and the incidence of cardiovascular events in patients with end-stage renal disease, as well as future renal injury in subjects with normal BP and renal function. Our recent data demonstrate that NE derived from renal nerves causes renal inflammation and fibrosis progression through alpha-2 adrenergic receptors (α₂-AR) in renal fibrosis models independent of BP. Sympathetic nerve activation-associated molecular mechanisms and signals seem to be critical for the development and progression of CKD, but the exact role of sympathetic nerve activation in CKD progression remains undefined. This review explores the current knowledge of NE-α₂-AR signaling in renal diseases and offers prospective views on developing therapeutic strategies targeting NE-AR signaling in CKD progression.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Plasma
/
Presión Sanguínea
/
Fibrosis
/
Daño por Reperfusión
/
Norepinefrina
/
Incidencia
/
Estudios Prospectivos
/
Receptores Adrenérgicos
/
Receptores Adrenérgicos alfa 2
/
Neurotransmisores
Tipo de estudio:
Estudio de incidencia
/
Estudio observacional
/
Estudio pronóstico
Límite:
Humanos
Idioma:
Inglés
Revista:
Kidney Research and Clinical Practice
Año:
2019
Tipo del documento:
Artículo
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