Lanthanum potentiation of the vascular response to a protein kinase C activator in genetically hypertensive rats

Jeffrey Raval, Irving G. Joshua, R Clinton Webb, David F. Bohr

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The effects of lanthanum on the contraction induced by the protein kinase C activator, 12-0-tetradecanoylphorbol-13-ac-etate (TPA) were studied in femoral artery rings from stroke- prone, spontaneously hypertensive rats (SHRSP) and normo- tensive Wistar-Kyoto rats (WKY). When exposed to a calcium- free buffer containing 1 mmol/l EGTA, the femoral artery rings from SHRSP and WKY, pre-contracted with TPA (10-6mol/l), relaxed by 52 and 24%, respectively. Treatment of the rings in this calcium-free buffer with 2.6 mmol/l lanthanum significantly potentiated the TPA-induced contractions in vascular rings from WKY (49%) and SHRSP (136%). Potentiation by lanthanum of the TPA-induced contraction in the absence of extracellular calcium suggests that this cation is acting intracellularly to increase protein kinase C activity. The in-creased vascular responsiveness of SHRSP to lanthanum may reflect an abnormality in protein kinase C activation in vascular smooth muscle of genetically hypertensive rats.

Original languageEnglish (US)
Pages (from-to)S146-S147
JournalJournal of Hypertension, Supplement
StatePublished - Jan 1 1989
Externally publishedYes



  • Calcium
  • Femoral artery
  • Genetic hypertension
  • Lanthanum
  • Protein kinase C activators

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

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