Effects of Pressor Substances on Low Density Lipoprotein Peroxidation by Cu++

Abstract

To investigate whether pressor substances accelerate low density lipoprotein peroxidation by Cu++, low density lipoprotein was dialysed against physiological saline containing O-5 mumol/l CuCl2 and/or 1 mumol/l of various pressor substances. Lipid peroxide value of low density lipoprotein changed little with the addition of norepinephrine to the saline, but the addition of norepinephrine to 1 mumol/l CuCl2 accelerated the peroxidation. When low density lipoprotein was dialysed against saline with norepinephrine, epinephrine, serotonin or dopamine, there were no significant differences in the lipid peroxide values of low density lipoprotein. Although the addition of serotonin into the dialyzate did not accelerate the peroxidation of low density lipoprotein due to Cu++, the addition of norepinephrine, epinephrine and dopamine accelerated the Cu(++)-peroxidation with a significant increase in the acceleration rate starting at the 36 hour point. Thus, it is speculated that various stresses stimulating the sympathetic nervous system accelerate the peroxidation of low density lipoprotein and produce peroxidized low density lipoprotein in the blood.

Effective blood pressure treatment improves LDL‐cholesterol susceptibility to oxidation in patients with essential hypertension

“…A direct effect of angiotensin II (independent of its vasoconstrictor effect) on vascular smooth muscle cells superoxide production has been demostrated [13]. Similarly, sympathetic agonists such as noradrenaline, adrenaline and dopamine stimulate LDL peroxidation in vitro [14]. These nonhaemodynamic pathways remain to be defined before they can be targeted by specific antihypertensive treatment.…”