C. Cardillo et al., IMPAIRMENT OF THE NITRIC OXIDE-MEDIATED VASODILATOR RESPONSE TO MENTAL STRESS IN HYPERTENSIVE BUT NOT IN HYPERCHOLESTEROLEMIC PATIENTS, Journal of the American College of Cardiology, 32(5), 1998, pp. 1207-1213
Objectives. This study investigated whether mental stress-induced vaso
dilation mediated by endothelium-derived nitric oxide (NO) is defectiv
e in conditions with endothelial dysfunction, such as hypertension and
hypercholesterolemia. Background. Vascular release of NO modulates th
e vasodilator response to mental stress in healthy subjects. Previous
studies have shown that hypertensive and hypercholesterolemic patients
have impaired endothelium-dependent vasodilation to pharmacologic age
nts due to decreased NO activity, However, whether this abnormality al
so operates in response to physiologic stimuli such as mental stress h
as not been defined. Methods. Forearm blood flow responses (plethysmog
raphy) to mental stress were compared in 12 normal subjects, 12 hypert
ensive patients and 10 hypercholesterolemic patients before and during
NO synthesis inhibition with N-G-monomethyl-L arginine (4 mu mol/min)
. Vascular responses to acetylcholine (7.5, 15 and 30 mu g/min), an en
dothelium-dependent vasodilator, and sodium ni troprusside (0.8, 1.6 a
nd 3.2 mu g/min), an exogenous NO donor, were also assessed in each gr
oup. Results. During saline the vasodilator response to mental stress
was significantly blunted in hypertensive (37 +/- 11%; p = 0.01) but n
ot in hypercholesterolemic (85 +/- 21%; p = 0.78) patients compared wi
th controls (93 +/- 15%), N-G-Monomethyl-L-arginine administration sig
nificantly blunted mental stress-induced vaso dilation in healthy subj
ects (p = 0.004 vs. saline) and hypercholesterolemic patients (p = 0.0
3 vs. saline), but not in hypertensive patients (p = 0.69 vs. saline).
The vasodilator effect of the highest dose of acetylcholine was simil
arly blunted in hypertensive (215 +/- 44%; p = 0.02) and hypercholeste
rolemic (172 +/- 71%; p = 0.02) patients compared with controls (364 /- 34), whereas the vasorelaxing response to sodium nitroprusside was
similar in the three groups. Conclusions. Hypertensive but not hyperch
olesterolemic patients have impaired NO-dependent vasodilation during
mental stress. These findings may be accounted for by different mechan
isms underlying endothelial dysfunction in these two conditions and mi
ght explain an increased susceptibility of hypertensive patients to va
scular damage over repeated exposure to stressful situations. (C) 1998
by the American College of Cardiology.