Pressure-independent contribution of sodium to large artery structure and function in hypertension

Sodium sensitivity is usually studied in terms of change of blood pressure (BP) but the specific effects on conduit arteries have not been addressed.

In genetic models of hypertension, chronically increased sodium diet is associated with aortic hypertrophy and development of extracellular matrix independent of BP. These alterations, often associated with increased stiffness and secretory properties of vascular smooth muscle, are reversed by lowering sodium intake and/or giving diuretics, independently of BP changes. The arterial changes are chronically modulated by hormonal counterregulatory mechanisms since, when sodium intake is high, bradykinin blockade produces more carotid hypertrophy, and when sodium intake is normal, less aortic collagen accumulates because of AT(1)-receptor blockade.

In longitudinal studies on hypertensive subjects, increased sodium intake not only increases BP but also decreases brachial artery diameter, implying pressure-independent mechanisms acting on the arterial wall. The antihypertensive effect of diuretics is associated with little change of arterial geometry and stiffness, probably resulting from marked angiotensin-induced increase of arterial stiffness. This latter effect is blocked by converting-enzyme inhibition. All these arterial changes may be genetically modulated since in salt-sensitive hypertensives, increased sodium intake is associated with decreased arterial distensibility, and in some hypertensive subjects, a polymorphism of the AT(1)-receptor gene has been described in association with increased aortic stiffness and is reversed by converting-enzyme inhibition independent of BP.

In genetic models of human and rat hypertension, increased sodium intake is associated with specific alterations of the structure and function of conduit arteries involving extracellular matrix, but independent of BP and atherosclerosis.