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Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2348-2354
Published online before print September 6, 2007, doi: 10.1161/ATVBAHA.107.147991
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2348.)
© 2007 American Heart Association, Inc.


Vascular Biology

Adaptation of Vasomotor Function of Human Coronary Arterioles to the Simultaneous Presence of Obesity and Hypertension

Tibor Fulop; Eva Jebelovszki; Nora Erdei; Tamas Szerafin; Tamas Forster; Istvan Edes; Akos Koller; Zsolt Bagi

From the Institute of Cardiology (T.F., N.E., T.S., I.E., Z.B.), University of Debrecen, Hungary; the 2nd Department of Medicine and Center of Cardiology (E.J., T.F.), University of Szeged, Hungary; and the Department of Physiology (A.K., Z.B.), New York Medical College, Valhalla, NY.

Correspondence to Zsolt Bagi, MD, PhD, Institute of Cardiology, University of Debrecen, Moricz Zs. Krt. 22, 4032-Debrecen, Hungary. E-mail bagizs{at}dote.hu

Objectives— We hypothesized that simultaneous presence of obesity and hypertension activates adaptive vascular mechanisms affecting dilations of human coronary arterioles.

Methods and Results— Agonist-induced dilations were assessed in isolated pressurized coronary arterioles from patients (n=38) who underwent cardiac surgery. Among normotensives we found that dilations to bradykinin (BK) and the NO-donor, sodium-nitroprusside (SNP) were reduced in obese subjects (BK, 10–7 mol/L, lean:90±4%, obese:64±7%; SNP, 10–6 mol/L, lean:89±7%, obese:76±5%). However, among hypertensives, both BK- and SNP-induced dilations were significantly enhanced in obese patients, when compared with lean individuals (BK, lean:71±7%, obese:85±3%; SNP, lean:60±6%, obese:83±2%). Correspondingly, in hypertensive patients, but not in those of normotensives, a positive correlation was found between body mass index (BMI) and BK-induced (P=0.036, r=0.46), and also SNP-evoked (P=0.031, r=0.44) coronary dilations. Moreover, in additional 55 hypertensive patients flow-mediated (FMD) and nitroglycerin (NTG)-induced dilations of the brachial artery were assessed. In obese hypertensive individuals, FMD- and NTG-induced dilations were greater (FMD:6.2±0.7%, NTG:17.2±0.9%), than in lean hypertensive patients (FMD:3.7±0.6%, NTG:13.6±1.1%). Correspondingly, FMD- and NTG-induced dilations were positively correlated with BMI (P=0.020, r=0.31 and P=0.033, r=0.29, respectively).

Conclusions— These findings are the first to suggest that obesity may lead to activation of adaptive vascular mechanisms to enhance the dilator function of coronary and peripheral arterial vessels in hypertensive patients.

The present study shows enhanced dilations of coronary arterioles and brachial arteries in obese hypertensive patients, implying an important functional adaptation, such as an increased sensitivity to NO of coronary and peripheral arterial vessels, to the simultaneous presence of obesity and hypertension.


Key Words: obesity • hypertension • coronary microcirculation • flow-mediated dilation • nitrate




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