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One of the characteristics of hypertension is an impairment in arterial hemodynamics. Any definition of hypertension has to take account of oscillatory fluctuations during the cardiac cycle, that is, fluctuations in systolic and diastolic blood pressure around mean arterial pressure. These fluctuations are determined by ventricular ejection, arterial distensibility and the timing of arterial wave reflections.Larger arteries stiffen progressively with age, due to medial and intimal thickening. This alteration can be described as a decrease in arterial distensibility ( Di=δD/δP×D, where D is the diameter of the artery and P is the blood pressure). The most obvious consequence of arterial stiffening is an increase in the amplitude of pulse pressure, caused by an increase in systolic pressure and a decrease in diastolic pressure. Two mechanisms underlie this increase in pulse pressure: a higher incident pressure wave generated by the left ventricle into a stiffened aorta and an increase in the velocity of the pressure wave traveling forward and back in the arterial tree. In young subjects, the reflected wave causes an increase in the early diastolic wave, but in older people the reflected wave is summed with a late systolic wave, causing a dramatic increase in central systolic pressure. These phenomena affect left ventricular function adversely, increasing myocardial oxygen consumption and tending to decrease coronary blood flow. Furthermore, the increased systolic blood pressure induces left ventricular hypertrophy.Although all classes of antihypertensive drugs can reduce blood pressure, only some can decrease arterial distensibility. Angiotensin converting enzyme inhibitors and calcium antagonists have been shown to decrease the stiffness of conduit arteries and dilate peripheral arteries. This may account for the superiority of these drugs in regressing left ventricular hypertrophy.