Abstract

An indirect approach for the study of the changes in the incremental circumferential modulus (E) of the brachial artery after arteriolar vasodilatation was undertaken in patients with sustained essential hypertension. The product of E and the thickness (h) of the arterial wall was evaluated by means of the Moens-Korteweg equation using determinations of brachioradial pulse wave velocity and brachial artery diameter with pulsed Doppler methods. In three homogeneous groups of patients with hypertension the Eh product was studied after vasodilatation caused either by nitrendipine, a calcium entry blocking agent, or by medroxalol, an alpha and beta blocking agent, or by isosorbid dinitrate. The three drugs caused similar reductions in blood pressure and increases in arterial diameter and hence decreases in wall thickness. Variance analysis for multigroups indicated that the decrease in Eh after vasodilatation was significant for nitrendipine but not for medroxalol and isosorbid dinitrate. Covariance analysis showed that for any level in Eh product the decrease in Eh was higher for nitrendipine than for isosorbid dinitrate and medroxalol. Since the three drugs had comparable mechanical and geometrical effects, the study provided evidence that, in men with essential hypertension, the smooth muscle tone of the brachial artery was significantly more sensitive to calcium inhibition than to autonomic blockade, causing a more important decrease in elastic modulus.

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