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Until recently, investigators in the field of hypertension have focused primarily on the role played by mean arterial pressure in alterations of vascular structure during chronic hypertension. In this issue of Hypertension, Christensen considers the possible role of pulse pressure. The author measured mean arterial pressure, systolic pressure, diastolic pressure, pulse pressure, and heart rate in awake spontaneously hypertensive rats (SHR) that had been treated with perindopril or captopril (angiotensin I converting enzyme inhibitors), isradipine (a calcium antagonist), hydralazine (a vasodilator), or metoprolol (a /3,-blocker). Structural characteristics were determined in small mesenteric arteries using an in vitro approach. Care was taken to standardize both the location from which arteries were obtained and the conditions under which the cross-sectional area of the wall and luminal circumference were determined. All parameters of blood pressure and media/lumen ratio of small arteries were greater in untreated SHR than in WistarKyoto (WKY) rats. Whereas each of the antihypertensive treatments significantly reduced all parameters of blood pressure in SHR (except for metoprolol, which did not lower pulse pressure), only perindopril and isradipine significantly reduced the media/lumen ratio. The correlation between individual parameters of blood pressure and media/lumen ratio was stronger for pulse pressure than for systolic blood pressure, mean blood pressure, or diastolic blood pressure. These findings led Christensen to speculate that reduction of pulse pressure during antihypertensive treatment may be a factor in prevention of altered vascular structure during chronic hypertension. Christensen's findings have important implications in relation to determinants of vascular structure. Alterations of vascular structure during chronic hypertension have been linked to a variety of determi-

Is pulse pressure a stimulus for altered vascular structure in chronic hypertension?