Hypertension, small arteries, and pathways for angiotensin II generation: "The proper study of mankind is man".

Abstract

In his seminal review, Folkow1 pointed out that recognition of structural cardiovascular changes in association with hypertension is longstanding: In 1836, Richard Bright described both left ventricular and aortic wall thickening in Bright’s disease. Moreover, George Johnson some 50 years later first reported wall thickening in arterioles, but the functional and hemodynamic consequences appear to have been overlooked until Folkow began to develop the theme some 30 years ago, a field of interest that has grown over the past 3 decades. Until about 10 to 15 years ago, the underlying pathogenetic sequence seemed straightforward. Muscle hypertrophies in the face of an increased workload. An increase in arterial blood pressure represents an increase in workload for the heart and the arterial tree. Hypertrophy of the heart and vascular tree, then, not only come as no surprise but might have been anticipated. If elevated blood pressure represents the central element in pathogenesis, why does control of blood pressure with the β-blocking agent atenolol not reverse the hypertrophic process in the study by Schiffrin et al in this issue of Circulation and earlier studies?2 3 The ratio of small-artery wall thickness to lumen was as increased after a year of treatment with atenolol as it was at baseline. It has been …