Mechanical function and histological structure of the arterial wall. The response to antihypertensive treatment

Alterations in the structure and function of large arteries could be a major factor in the mortality and morbidity of hypertensive patients. This paper summarises the effects of various pharmacological treatments on the mechanical (functional) properties of large arterial walls and on the structure and composition of these vessels. Firstly, during arterial hypertension, increases in arterial stiffness, associated with medial hypertrophy and/or hyperplasia and alterations in extracellular matrix, are always observed. Sodium intake and aging may influence the arterial wall properties, causing an increase in stiffness, independently of their effect on blood pressure. In parallel, administration of low doses of diuretics to hypertensive rats did not cause significant haemodynamic changes, but did cause an increase in arterial distensibility. Nitrates and derivatives have specific effects on the smooth muscle from large arteries in hypertensive patients. Significant increases in the diameter of large arteries and in arterial wall stiffness have been reported in clinical studies, but these effects have a short time constant. In humans and animals, angiotensin converting enzyme (ACE) inhibitors and calcium antagonists cause relaxation of arterial smooth muscle and, therefore, improve the functional component of the reduced distensibility observed in hypertension. Long term treatment with ACE inhibitors and calcium antagonists induces a significant reduction in medial hypertrophy. However, it is difficult to distinguish between the direct effects resulting from pressure reduction and a specific drug effect.