Sodium, large arteries, and diuretic compounds in hypertension.
Clinical and experimental data have shown that antihypertensive drugs do not cause the same change in arterial compliance for an equipotent blood pressure reduction. However, there is not clear data on the effect of sodium and diuretics on the visco-elastic properties of the hypertensive arterial wall. Cross-sectional epidemiologic studies suggest that, at any given value of age and blood pressure, pulse wave velocity is lower in the presence of decreased sodium intake. Longitudinal studies indicate that, in hypertensive subjects, low sodium intake is associated with a larger brachial artery diameter than is high sodium intake. In hypertension in the elderly and in severe hypertension with end-stage renal disease, sodium overload causes a reduction in arterial compliance and distensibility unrelated to blood pressure changes. In animal studies, the diuretic compounds cycletanine and indapamide were shown to increase systemic and carotid compliance independently of blood pressure changes. In contrast, a crossover study of hypertensive subjects showed that the diuretic agent hydrochlorothiazide did not change arterial compliance and pulse wave velocity, whereas the calcium entry blocker, felodipine, improved these parameters. Nevertheless, indapamide decreased the pulse pressure on stroke volume ratio, a parameter used as a marker of aortic distensibility. Taken together, such studies indicate that sodium may act on the arterial wall independently of blood pressure changes. The contribution of counter regulatory mechanisms, possibly related to the renin-angiotensin and sympathetic nervous systems, might explain the differences between the clinical and experimental changes observed with diuretic compounds. Of the various antihypertensive agents, diuretics seem to have the least effect on the arterial system.
Safar
M E
ME
Department of Internal Medicine, Broussais Hospital, Paris, France.
Asmar
R
R
Benetos
A
A
Levy
B I
BI
London
G M
GM
D000818:Animals; D001158:Arteries / Q000187:drug effects* / Q000503:physiopathology; D004232:Diuretics / Q000494:pharmacology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D012964:Sodium / Q000494:pharmacology*
D004232:Diuretics; D012964:Sodium