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September 1, 1996The Journal of PhysiologyOpen Access

Angiotensin II activation of protein kinase C decreases delayed rectifier K+ current in rabbit vascular myocytes.

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Population

Isolated rabbit portal vein smooth muscle cells (myocytes)

Comparison

Angiotensin II (100 nM) vs Baseline/washout or presence of antagonists

Design

Preclinical

Authors

OCOdile Clément‐ChomienneUniversité Paris-SudMWMichael P. WalshUniversity College DublinWCW. C. ColeUniversity of Nevada, Reno

Discussion

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Implication

Hypothesis-generating for PKC-ε mediation of Ang II effects on vascular excitability; leaves open human translation and should not change practice.

Key Points

  • To investigate the effect of angiotensin II on delayed rectifier K+ currents in isolated vascular smooth muscle cells and determine the underlying signal transduction pathway.
  • Recorded macroscopic whole-cell delayed rectifier K+ currents (IK(V)) in isolated rabbit portal vein smooth muscle cells exposed to 100 nM angiotensin II at 20°C and 30°C using whole-cell voltage clamp.
  • Assessed signaling mechanisms using the AT1 receptor antagonist losartan (1 µM), extracellular Ca2+ substitution with Mg2+, and selective PKC inhibitors calphostin C (1 µM) and chelerythrine (50 µM).
  • Characterized the expression of PKC isoenzymes in rabbit portal vein tissue using isoenzyme-specific antibodies.
  • Angiotensin II reduced IK(V) tail current from 3.9 ± 0.7 to 2.5 ± 0.5 pA/pF at 20°C (n=6) and from 4.5 ± 0.5 to 3.13 ± 0.4 pA/pF at 30°C (n=17), an effect fully reversed upon washout.
  • Angiotensin II accelerated the rapid phase of current inactivation (tau 1 decreased from 377 ± 32 to 245 ± 11 ms; n=17) without altering voltage dependence of activation or inactivation.
  • Current inhibition was prevented by losartan, calphostin C, and chelerythrine, and persisted in Ca2+-free conditions, implicating the Ca2+-independent PKC-epsilon isoform identified in portal vein tissue.

Structured PICO

P
Population
Isolated rabbit portal vein smooth muscle cells (myocytes)
I
Intervention
Angiotensin II (100 nM)
C
Comparator
Baseline/washout or presence of antagonists (losartan, calphostin C, chelerythrine)
O
Outcome
Delayed rectifier K+ current (IK(V))surrogate

Angiotensin II decreases delayed rectifier K+ current in rabbit vascular myocytes via activation of protein kinase C, likely the calcium-independent epsilon isoenzyme.

Cite This Study

Clément‐Chomienne et al. (1996) studied this question.

synapsesocial.com/papers/6a70dcd58031ec7bb1dca266https://doi.org/10.1113/jphysiol.1996.sp021626
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Protein kinase C inhibits delayed rectifier K+ current in rabbit vascular smooth muscle cells1996 · 80 citations
  2. 2A role for protein kinase C‐ϵ in angiotensin II stimulation of phospholipase D in rat renal mesangial cells1993 · 35 citations
  3. 3Control of resting membrane potential by delayed rectifier potassium currents in ferret airway smooth muscle cells.1993 · 86 citations
  4. 4Vascular smooth-muscle cells contain AT1 angiotensin receptors coupled to phospholipase D activation1994 · 50 citations
  5. 5Cloning and expression of a Kv1.2 class delayed rectifier K+ channel from canine colonic smooth muscle.1993 · 80 citations