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Clinical Trial
. 1996 Oct;14(10):1247-55.
doi: 10.1097/00004872-199610000-00014.

Structure and function of resistance arteries of hypertensive patients treated with a beta-blocker or a calcium channel antagonist

Affiliations
Clinical Trial

Structure and function of resistance arteries of hypertensive patients treated with a beta-blocker or a calcium channel antagonist

E L Schiffrin et al. J Hypertens. 1996 Oct.

Abstract

Objective: To investigate the effects on resistance artery structure and function of monotherapy with the beta-blocker atenolol or the calcium channel antagonist nifedipine in its once a day form or gastrointestinal therapeutic system (GITS).

Subjects: Twenty well-controlled essential hypertensive patients matched for age, body mass index, duration and severity of hypertension. Normotensive subjects and untreated hypertensives served as the reference groups.

Methods: Resistance-size small arteries (standardized lumen diameter 247 +/- 8 microns) were dissected from a gluteal subcutaneous biopsy, and studied both on a wire myograph as pressurized vessels.

Results: The media width:lumen diameter ratio of arteries was 5.37 +/- 0.09% in normotensive subjects, 5.38 +/- 0.18% in patients treated with nifedipine GITS, 6.81 +/- 0.18% in patients treated with atenolol and 7.08 +/- 0.12% in untreated hypertensives (for each of the latter two groups P < 0.001, versus each of the two former groups). The media stress developed in response to noradrenaline and the endothelium-dependent relaxation induced by acetylcholine were significantly smaller in small arteries from untreated or atenolol-treated patients than they were in those from normotensive subjects or nifedipine GITS-treated patients.

Conclusion: Hypertensive patients with well-controlled blood pressures under treatment for more than 1 year with the once-a-day calcium channel antagonist nifedipine GITS exhibit normal structure and function of gluteal subcutaneous small arteries, whereas similar patients with blood pressure equally well controlled by the beta-blocker atenolol present thicker small arteries with abnormal endothelium-dependent relaxation and altered contractility. Whether this finding applies also to other vascular beds, and whether it is associated with a better outcome in relation to morbidity and mortality resulting from elevated blood pressure, remain to be established.

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