Renal neurohormonal regulation in heart failure decompensation

Am J Physiol Regul Integr Comp Physiol. 2014 Sep 1;307(5):R493-7. doi: 10.1152/ajpregu.00178.2014. Epub 2014 Jun 11.

Abstract

Decompensation in heart failure occurs when the heart fails to balance venous return with cardiac output, leading to fluid congestion and contributing to mortality. Decompensated heart failure can cause acute kidney injury (AKI), which further increases mortality. Heart failure activates signaling systems that are deleterious to kidneys such as renal sympathetic nerve activity (RSNA), renin-angiotensin-aldosterone system, and vasopressin secretion. All three reduce renal blood flow (RBF) and increase tubular sodium reabsorption, which may increase renal oxygen consumption causing AKI through renal tissue hypoxia. Vasopressin contributes to venous congestion through aquaporin-mediated water retention. Additional water retention may be mediated through vasopressin-induced medullary urea transport and hyaluronan but needs further study. In addition, there are several systems that could protect the kidneys and reduce fluid retention such as natriuretic peptides, prostaglandins, and nitric oxide. However, the effect of natriuretic peptides and nitric oxide are blunted in decompensation, partly due to oxidative stress. This review considers how neurohormonal signaling in heart failure drives fluid retention by the kidneys and thus exacerbates decompensation. It further identifies areas where there is limited data, such as signaling systems 20-HETE, purines, endothelin, the role of renal water retention mechanisms for congestion, and renal hypoxia in AKI during heart failure.

Keywords: ADHF; GFR; acute renal failure; cardiorenal syndrome; glomerular filtration rate.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Kidney Injury / etiology
  • Acute Kidney Injury / physiopathology
  • Animals
  • Cardiac Output / physiology
  • Heart Failure / complications
  • Heart Failure / physiopathology*
  • Humans
  • Kidney / innervation
  • Kidney / physiology*
  • Neurotransmitter Agents / physiology*
  • Signal Transduction / physiology
  • Sympathetic Nervous System / physiology
  • Water-Electrolyte Balance / physiology

Substances

  • Neurotransmitter Agents