Sodium, large arteries and diuretic compounds in hypertension.
BACKGROUND
Clinical and experimental data have shown that different antihypertensive drugs do not cause similar changes in arterial compliance for an equipotent blood pressure reduction. There are no clear data on the effects of sodium and diuretics on the visco-elastic properties of the hypertensive arterial wall.


METHODS
Cross-sectional epidemiological studies suggest that for given values of age and blood pressure, pulse wave velocity is lower in the presence than in the absence of a low sodium intake. Longitudinal studies indicate that in hypertensive subjects, a low sodium intake is associated with a larger brachial artery diameter than that seen with a high sodium intake. In hypertension in the elderly and in severe hypertension with end-stage renal disease, a sodium overload reduces arterial compliance and distensibility independently of blood pressure changes. In animal studies, the diuretic compounds cycletanine and indapamide increase systemic and carotid compliance independently of blood pressure changes. In contrast, in a crossover study in hypertensive subjects, the diuretic agent hydrochlorothiazide did not change arterial compliance and pulse wave velocity while the calcium entry-blocker felodipine did improve these hemodynamic parameters.


CONCLUSIONS
The studies reviewed indicate that sodium may act on the arterial wall independently of blood pressure changes. the contribution made by counter-regulatory mechanisms, which may be related to the renin-angiotensin and the sympathetic nervous systems, might explain the differences between the clinical and the experimental changes observed with diuretic compounds.
Safar
M E
ME
Department of Internal Medicine, Broussais Hospital, Paris, France.
Asmar
R G
RG
Benetos
A
A
London
G M
GM
Lévy
B I
BI
D000818:Animals; D001158:Arteries / Q000187:drug effects*; D003187:Compliance / Q000187:drug effects; D004232:Diuretics / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D012964:Sodium / Q000494:pharmacology*
D004232:Diuretics; D012964:Sodium