Interleukin-10 inhibits angiotensin II-induced decrease in neuronal potassium current.

Academic Article


  • Previously we demonstrated that viral-mediated increased expression of the anti-inflammatory cytokine interleukin-10 within the paraventricular nucleus of the hypothalamus significantly reduces blood pressure in normal rats made hypertensive by infusion of angiotensin II. However, the exact cellular locus of this interleukin-10 action within the paraventricular nucleus is unknown. In the present study we tested whether interleukin-10 exerts direct effects at its receptors located on hypothalamic neurons to offset the neuronal excitatory actions of angiotensin II via its type 1 receptors. The results indicated the presence of immunoreactive interleukin-10 receptors on neurons in normal rat paraventricular nucleus and that receptors for this cytokine were also expressed in neurons cultured from the hypothalamus. Patch-clamp electrophysiological recordings from these cultures revealed that extracellular application of interleukin-10 alone did not exert any alterations in neuronal membrane delayed rectifier or transient potassium currents. However, angiotensin II elicited a significant decrease in delayed rectifier potassium current, an effect that was abolished by interleukin-10 application. Since decreases in delayed rectifier potassium current contribute to increased neuronal excitability, this result is consistent with a direct inhibitory action of interleukin-10 on angiotensin-induced excitation of hypothalamic neurons. As such, these data are the first indication of a neuronal locus of action of interleukin-10 to temper the actions of angiotensin II in the hypothalamus.
  • Authors


  • Angiotensin II, Animals, Cells, Cultured, Hypothalamus, Interleukin-10, Male, Membrane Potentials, Neurons, Potassium Channels, Rats, Rats, Sprague-Dawley, Receptors, Interleukin-10
  • Digital Object Identifier (doi)

    Author List

  • Jiang N; Shi P; Desland F; Kitchen-Pareja MC; Sumners C
  • Start Page

  • C801
  • End Page

  • C807
  • Volume

  • 304
  • Issue

  • 8