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


METHODS
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.


CONCLUSIONS
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.
Schiffrin
E L
EL
MRC Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montréal, Hôtel-Dieu de Montréal Hospital, University of Montréal, Quebec, Canada.
Deng
L Y
LY
D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage*; D000328:Adult; D000368:Aged; D001158:Arteries / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology*; D001262:Atenolol / Q000008:administration & dosage*; D002121:Calcium Channel Blockers / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D006984:Hypertrophy; D008297:Male; D016555:Matched-Pair Analysis; D008875:Middle Aged; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000473:pathology* / Q000503:physiopathology; D009543:Nifedipine / Q000008:administration & dosage*; D014655:Vascular Resistance
D000319:Adrenergic beta-Antagonists; D002121:Calcium Channel Blockers; D001262:Atenolol; D009543:Nifedipine