ATHEROGENIC LIPOPROTEINS INHIBIT CATECHOLAMINE SECRETION IN CULTURED BOVINE ADRENAL-MEDULLARY CELLS

The effects of lipoproteins on ion channel-mediated catecholamine secr etion were investigated in cultured bovine adrenal medullary cells. Lo w density lipoprotein (LDL, 20-80 mg/dl) and lipoprotein(a) [Lp(a); 10 -80 mg/dl] inhibited catecholamine secretion induced by carbachol, an activator of nicotinic acetylcholine receptor-ion channels. LDL and Lp (a) suppressed carbachol-induced Na-22(+) influx as well as Ca-45(2+) influx in a concentration-dependent manner similar to that of catechol amine secretion. The inhibition of catecholamine secretion by Lp(a) wa s not overcome by increasing the concentration of carbachol. On the ot her hand, high density lipoprotein (HDL; <150 mg/dl) had no effect on Na-22(+) influx, Ca-45(2+) influx, and catecholamine secretion. Like L DL and Lp(a), a synthetic peptide homologous to human plasma apolipopr otein B (apoB), apoB fragment(3358-3372)-amide (3-60 mu M), attenuated Na-22(+) influx, Ca-45(2+) influx, and catecholamine secretion caused by carbachol. The apoB fragment also suppressed Na-22(+) influx induc ed by veratridine tan activator of voltage-dependent Na+ channels) and Ca-45(2+) influx induced by 56 mM K+ tan indirect activator of voltag e-dependent Ca2+ channels). These findings suggest that atherogenic li poproteins such as LDL and Lp(a) suppress catecholamine secretion by i nterfering with Naf influx through nicotinic acetylcholine receptor-io n channels, in which apoB, a structural component common to both LDL a nd Lp(a), plays an important role. The inhibition by atherogenic lipop roteins of catecholamine secretion may influence the progression of at herosclerosis induced by these lipoproteins.