The baroreflex is a negative feedback system for regulation of blood pressure. Its sensors, the baroreceptors located in the aortic wall and the carotid sinuses, are, however, not pressure sensors, but mechanoreceptors excited by stretch. Here we present a computational physiology model which shows that the increase in arterial stiffness that follows with age is sufficient to account for an overwhelming amount of experimental and clinical data on hypertension. We demonstrate quantitatively that the stiffening causes the baroreceptors to misinform the highly complex machinery responsible for blood pressure regulation. This misinformation occurs because the baroreceptors are strain sensitive, not pressure sensitive, and with stiffening the aortic wall strain ceases to be a good proxy for aortic blood pressure. In contrast to widely held opinions, the results suggest that primary hypertension can be attributed to a mechanogenic etiology without challenging current conceptions of renal and sympathetic nervous system function. And they support the view that a major target for treating chronic hypertension in the elderly is the reestablishment of a proper baroreflex response.