Structure and Function of Resistance Arteries of Hypertensive Patients Treated with a Beta-blocker or a Calcium Channel Antagonist
Overview
Authors
Affiliations
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.
Systemic and Cardiac Microvascular Dysfunction in Hypertension.
Durante A, Mazzapicchi A, Baiardo Redaelli M Int J Mol Sci. 2025; 25(24.
PMID: 39769057 PMC: 11677602. DOI: 10.3390/ijms252413294.
Maruhashi T, Higashi Y Hypertens Res. 2022; 45(8):1322-1333.
PMID: 35595983 DOI: 10.1038/s41440-022-00936-x.
Brandt M, Cheng C, Merkus D, Duncker D, Sorop O Front Physiol. 2022; 12:771960.
PMID: 35002759 PMC: 8733629. DOI: 10.3389/fphys.2021.771960.
Assessment and pathophysiology of microvascular disease: recent progress and clinical implications.
Masi S, Rizzoni D, Taddei S, Widmer R, Montezano A, Luscher T Eur Heart J. 2020; 42(26):2590-2604.
PMID: 33257973 PMC: 8266605. DOI: 10.1093/eurheartj/ehaa857.
Masi S, Georgiopoulos G, Alexopoulos G, Pateras K, Rosada J, Seravalle G J Clin Med. 2020; 9(7).
PMID: 32605201 PMC: 7409082. DOI: 10.3390/jcm9072027.