Regional changes in cardiac and stellate ganglion norepinephrine transporter in DOCA-salt hypertension

Erica A. Wehrwein, Martin Novotny, Greg M. Swain, Lindsay M. Parker, Mohammad Esfahanian, John M. Spitsbergen, Beth A. Habecker, David L. Kreulen

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Uptake of norepinephrine via the neuronal norepinephrine transporter is reduced in the heart during deoxycorticosterone (DOCA)-salt hypertension. We hypothesized that this was due to reduced norepinephrine transporter mRNA and/or protein expression in the stellate ganglia and heart. After 4. weeks of DOCA-salt treatment there was no change in norepinephrine transporter mRNA in either the right or the left stellate ganglia from hypertensive rats (n = 5-7, p > 0.05). Norepinephrine transporter immunoreactivity in the left stellate ganglion was significantly increased (n = 4, p. < 0.05) while the right stellate ganglion was unchanged (n = 4, p > 0.05). Whole heart norepinephrine content was significantly reduced in DOCA rats consistent with reduced uptake function; however, when norepinephrine was assessed by chamber, a significant decrease was noted only in the right atrium and right ventricle (n = 6, p < 0.05). Cardiac norepinephrine transport binding by chamber revealed that it was only reduced in the left atrium (n = 5-7, p > 0.05). Therefore, 1) contrary to our hypothesis reduced reuptake in the hypertensive heart is not exclusively due to an overall reduction in norepinephrine transporter mRNA or protein in the stellate ganglion or heart, and 2) norepinephrine transporter regulation occurs regionally in the heart and stellate ganglion in the hypertensive rat heart.

Original languageEnglish (US)
Pages (from-to)99-107
Number of pages9
JournalAutonomic Neuroscience: Basic and Clinical
Volume179
Issue number1-2
DOIs
StatePublished - Dec 2013

Keywords

  • Cardiac
  • Hypertension
  • NAT
  • NET
  • Noradrenaline
  • Stellate ganglion

ASJC Scopus subject areas

  • Endocrine and Autonomic Systems
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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