To understand the role of endothelially derived vasospastic superoxide
anion (SO) and vasodilatory nitric oxide (NO) in vascular disorders s
uch as essential hypertension (EHT) and atherosclerosis, malondialdehy
de (MDA), a stable end product of lipid peroxidative damage, and nitri
te, mostly derived from NO, have been estimated in the serum of hypert
ensive patients and in patients suffering from myocardial ischaemia (s
table or unstable angina or acute myocardial infarction (AMI)). An inc
rease in serum MDA together with a decline in serum nitrite was observ
ed in patients with EHT, indicating respectively heightened activity o
f oxygen free radicals (OFR) and diminished NO production. Similarly,
patients with stable or unstable angina or AMI had elevated levels of
serum MDA while serum nitrite declined only in unstable angina and AMI
. These changes in MDA and nitrite probably occurred as a result of an
endothelial response to extravascular factors such as angiotensin II
and dyslipidaemia or mere endothelial dysfunction in EHT and atheroscl
erosis. In these patients, other disease states such as diabetes, arth
ritis and other inflammatory disorders associated with OFR generation
were excluded.