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

The effects of lanthanum on the contraction induced by the protein kinase C activator, 12-O-tetradecanoylphorbol-13-acetate (TPA) were studied in femoral artery rings from stroke-prone, spontaneously hypertensive rats (SHRSP) and normotensive 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(-6) mol/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 increased vascular responsiveness of SHRSP to lanthanum may reflect an abnormality in protein kinase C activation in vascular smooth muscle of genetically hypertensive rats.