AJP - Cell Physiology, Vol 262, Issue 6 C1376-C1383, Copyright © 1992 by American Physiological Society
Norepinephrine-induced phosphatidylcholine hydrolysis by phospholipases D and C in rat tail artery
H. Gu, S. Trajkovic and E. F. LaBelle
Bockus Research Institute, Graduate Hospital, Philadelphia, Pennsylvania 19146.
Rat tail arterial segments were incubated with [3H]choline to selectively
label endogenous phosphatidylcholine. Norepinephrine (NE; 10(-5) M)
addition for periods of 10 s to 30 min significantly increased the
concentration of extracellular phosphatidylcholine metabolites,
[3H]choline, and [3H]phosphocholine. The release of [3H]choline and
[3H]phosphocholine from the segments was NE dose dependent (10(-6)-10(-3)
M). NE also increased the formation of [3H]phosphatidylethanol in
[3H]myristate-labeled tail artery in the presence of ethanol,
characteristic of phospholipase D activity. NE-induced phosphatidylcholine
hydrolysis was blocked by pretreatment with prazosin (10(-5) M) and was
unchanged by pretreatment with propranolol (10(-5) M). 4 beta-phorbol
12,13-dibutyrate (PDBu, 10(-6) M) stimulated the release of [3H]choline,
which was inhibited by pretreatment with staurosporine (10(-5) M). The
stimulatory effect of NE on phosphatidylcholine metabolism was not altered
by either pretreatment with staurosporine (10(-5) M) or calcium-free
buffer. In summary, we have demonstrated NE-stimulated phosphatidylcholine
hydrolysis by phospholipase D and C in intact vascular smooth muscle. This
effect of NE was dose dependent and was mediated through the alpha
1-adrenergic receptor. Norepinephrine and PDBu stimulated
phosphatidylcholine hydrolysis through different mechanism(s), and the
stimulatory effect of NE did not seem to require protein kinase C and
calcium influx.
