Activation of calcium sparks by angiotensin II in vascular myocytes

Biochem Biophys Res Commun. 1996 May 24;222(3):809-15. doi: 10.1006/bbrc.1996.0808.


Contraction in smooth muscle is triggered by an increase in cytoplasmic free calcium ([Ca2+]i) which depends on both Ca2+ influx through L-type Ca2+ channels and Ca2+ release from the sarcoplasmic reticulum (SR). Two mechanisms have been shown to be involved in SR Ca2+ release, one is stimulated by Ca2+ and involved ryanodine-sensitive Ca2+-release channels; the other is stimulated by an increase in inositol 1,4,5-trisphosphate (InsP3) generation induced by various mediators and involved InsP3-sensitive Ca2+ release channels. Here, we examined the effects of angiotensin II on [Ca2+]i in single rat portal vein myocytes using both the whole cell patch-clamp method and a laser scanning confocal microscope. Elementary Ca2+ release events (Ca2+ sparks) were obtained spontaneously or in response to L-type Ca2+ channel current activation, and resulted from activation of ryanodine-sensitive Ca2+-release channels in the SR. We show that angiotensin AT1 receptors stimulate Ca2+ sparks through activation of L-type Ca2+ channels without involving InsP3-induced Ca2+ release. This novel transduction pathway may be a common mechanism for vasoconstrictors which do not stimulate generation of chemical second messengers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Calcium / metabolism*
  • Calcium Channels / metabolism*
  • Cells, Cultured
  • Dihydropyridines / pharmacology
  • Ion Channel Gating / drug effects
  • Membrane Potentials
  • Muscle, Smooth, Vascular / metabolism*
  • Patch-Clamp Techniques
  • Portal Vein
  • Rats
  • Rats, Wistar
  • Receptors, Angiotensin / physiology*


  • Calcium Channels
  • Dihydropyridines
  • Receptors, Angiotensin
  • Angiotensin II
  • oxodipine
  • Calcium