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Sympathetic Overactivity in CKD Disrupts Buffering of Neurotransmission by Endothelium-Derived Hyperpolarizing Factor

Wei Cao1, Liling Wu1, Xiaodong Zhang1

  • 1Division of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, People's Republic of China.

Journal of the American Society of Nephrology : JASN
|July 4, 2020
PubMed

Insights

Hypertension in chronic kidney disease (CKD) involves enhanced sympathetic nerve activity that impairs a protective anticontractile response, leading to increased vasoconstriction before structural changes occur.

Area of Science:

  • Nephrology
  • Cardiovascular Physiology
  • Neuroendocrinology

Background:

  • Hypertension is a common complication of chronic kidney disease (CKD).
  • Sympathetic nervous system signals normally induce an endothelial cell (EC)-dependent anticontractile response in resistance arteries, moderating vasoconstriction.
  • The role of this pathway in CKD-related vasoconstriction is not well understood.

Purpose of the Study:

  • To investigate the hypothesis that an impaired anticontractile mechanism enhances sympathetic vasoconstriction in a mouse model of CKD hypertension.
  • To elucidate the neurovascular mechanisms underlying enhanced vasoconstriction in CKD.

Main Methods:

  • A 5/6-nephrectomy (5/6Nx) mouse model of CKD hypertension was utilized.
  • Studies employed in vivo, ex vivo (isolated mesenteric arteries), and in vitro (VSMC and EC coculture) models.
  • Neurovascular transmission and its contribution to vascular resistance were assessed.

Main Results:

  • CKD mice exhibited increased vascular resistance and blood pressure, decreased connexin 43 (Cx43) expression at myoendothelial junctions (MEJs), and impaired EC-dependent hyperpolarization (EDH).
  • Exposure to norepinephrine reduced MEJ Cx43 and gap junction function in cocultures, preceding structural changes.
  • Inhibition of sympathetic outflow or Cx43 transfection normalized neurovascular transmission and vasoconstriction.

Conclusions:

  • CKD is associated with enhanced neurovascular transmission and vasoconstriction due to an impaired EDH anticontractile mechanism.
  • This impairment involves reduced Cx43 expression at MEJs, interrupting EDH responses.
  • Dysregulation of neurovascular transmission may contribute to hypertension development in CKD.
Abstract

Keywords:
chronic kidney diseaseconnexin 43hypertensionneurovascular transmissionsympathetic nervous system

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