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Sodium nitroprusside and cGMP decrease Ca2+ channel availability in basilar artery smooth muscle cells

K Tewari1, J M Simard

  • 1University of Maryland School of Medicine, Baltimore MD 21201, USA.

Pflugers Archiv : European Journal of Physiology
|January 1, 1997
PubMed
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Sodium nitroprusside (SNP), a nitric oxide (NO) donor, reduces calcium channel activity in guinea pig basilar artery smooth muscle cells. This effect involves cGMP-dependent protein kinase, not changes in channel properties.

Area of Science:

  • Cardiovascular Physiology
  • Smooth Muscle Biology
  • Ion Channel Function

Background:

  • Nitric oxide (NO) plays a crucial role in regulating vascular tone.
  • Calcium (Ca2+) channels are key determinants of smooth muscle contraction.
  • The precise mechanisms by which NO influences Ca2+ channels in the basilar artery remain incompletely understood.

Purpose of the Study:

  • To investigate the effect of the NO donor sodium nitroprusside (SNP) on Ca2+ channel currents in guinea pig basilar artery smooth muscle cells.
  • To elucidate the role of cyclic guanosine monophosphate (cGMP) and associated kinases in mediating NO's effects on these channels.

Main Methods:

  • Whole-cell patch-clamp recordings were used to measure macroscopic Ca2+ currents.
  • Cell-attached patch recordings were employed to analyze single Ca2+ channel activity.

Related Experiment Videos

  • The effects of SNP, 8-Br-cGMP, H-8 (a protein kinase inhibitor), 8-Br-cAMP, and forskolin were assessed.

    • Main Results:

    • SNP significantly decreased macroscopic Ca2+ currents and single-channel availability in a dose-dependent manner.
    • SNP did not alter the biophysical properties of the Ca2+ channels, such as conductance or voltage dependence.
    • 8-Br-cGMP mimicked SNP's effect on channel availability, while the cGMP-dependent protein kinase inhibitor H-8 blocked SNP's action.
    • cAMP analogs did not affect SNP-induced changes in channel availability.

    Conclusions:

    • Nitric oxide reduces Ca2+ channel openings in basilar artery smooth muscle cells primarily by decreasing channel availability.
    • The mechanism likely involves the activation of cGMP-dependent protein kinase.
    • These findings highlight a novel signaling pathway for NO in regulating vascular smooth muscle function.