Abstract-Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Key Words: hypertension Ⅲ hypercholesterolemia Ⅲ cardiovascular reactivity Ⅲ plethysmography Ⅲ vascular damage B oth hypertension and hypercholesterolemia, which frequently occur together, 1,2 are independent risk factors for cardiovascular events, 3 induce vascular damage, 4 and affect coronary flow by impairing endothelium-mediated vasodilation. 5 Moreover, borderline-to-mild hypertensive subjects, in whom sympathetic overdrive and exaggerated cardiovascular stress reactivity have been shown, 6 tend frequently to have high total (TOT-C) and LDL cholesterol (LDL-C) levels. 7,8 Several studies have shown also that patients characterized by emotional alertness often present dyslipidemia, exaggerated cardiovascular reactivity, and hypertension. 9,10 In hemodynamic terms, borderline hypertensive subjects in the resting state fail to accommodate to increased cardiac output with appropriate vasodilation 11 and, during laboratory mental stress, do not proportionally adjust forearm blood flow (FBF) while their blood pressure (BP) significantly increases. 12 Sympathetic overactivity emanating from the central nervous system 11 also enhances the effects of local factors that are conducive to vascular damage, including shear stress and turbulence, endothelial dysfunction, and atherosclerotic lesions. 13 Therefore, hypertension and hypercholesterolemia, though independent cardiovascular risk factors, may share physiopathological features that can be related to vascular sympathetic overactivity.In clinical studies, antihypertensive treatment with angiotensin-converting enzyme inhibitors (ACEIs) 14,15 as well as cholesterol-lowering therapy with statins 16,17 were found to improve vasodilating properties and to reduce vascular damage. Nevertheless, to the best of our acknowledge, no study has investigated their effect on regional vascular stress response and vascular structure in hypercholesterolemic hypertensive subjects. The current study analyzed forearm vascular response to psychophysiological tasks in hypercho-

Many biological and psychological factors induce haemodynamic and extra-cardiovascular functional changes mediated by the autonomic nervous system. Pharmacological blood pressure reduction, as a neurovegetative stimulus, can change the arousal of the sympathetic nervous system. We evaluated the effects of two calcium channel blockers, verapamil and amlodipine, both administered as monotherapies, upon the sympathetic stress response in 23 randomized mild-to-moderate essential hypertensives (161 +/- 2/98 +/- 1 mmHg). Patients performed four stress tests (mental arithmetic, colour word Stroop, cold pressor and handgrip) while extracardiovascular and haemodynamic functions were assessed non-invasively at every heart beat, during baseline, stress and recovery phases. The sympathetic response was evaluated by computing the 'area-under-the-curve' (value x time) measured during the psychophysiological session. The session was repeated at run-in, after placebo and during treatment. After one month's treatment, baseline blood pressure was significantly reduced in patients treated with amlodipine (139 +/- 1/84 +/- 1 mmHg; P < 0.001) and verapamil (140 +/- 2/85 +/- 1 mmHg; P < 0.001). The emotional arousal (frontalis muscular contraction, skin conductance) was unchanged, but the cutaneous vascular response was reduced (P < 0.05) in patients treated with verapamil. No changes in systolic or diastolic blood pressure were detectable, but amlodipine increased the heart rate response (P < 0.05). In contrast, verapamil reduced the heart rate (P < 0.05) without depressing the cardiac output response, which was increased with amlodipine (P < 0.05). Total vascular resistance was significantly (P < 0.001) reduced with both the treatments. Consequently, functional cardiac load, expressed by pressure-rate product and cardiac power, was significantly enhanced with amlodipine and reduced with verapamil. In conclusion, the abnormal sympathetic stress response, which characterizes the hypertensive patient, might be affected by the choice of medication. Verapamil in particular, moderated emotional arousal, the vasoconstrictive response and reduced cardiac load without lowering cardiac output demands. In contrast, in patients treated with amlodipine, in whom the cardiac output response was increased, the pattern was reversed and the functional cardiac load was also increased.

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