IMPAIRMENT OF THE NITRIC OXIDE-MEDIATED VASODILATOR RESPONSE TO MENTAL STRESS IN HYPERTENSIVE BUT NOT IN HYPERCHOLESTEROLEMIC PATIENTS

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.