Characteristics of adrenoceptors in the human radial artery: Clinical implications,☆☆,,★★

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Abstract

Objectives: The radial artery has been suggested to be spastic. Endogenous and exogenous catecholamines and the use of β-blockers may be related to radial artery spasm, but the characteristics of adrenoceptors in this artery are unknown. This study was designed to characterize the α- and β-adrenoceptor in the human radial artery. Methods: Ring segments of the radial artery (n = 59) taken from patients undergoing coronary artery bypass grafting were studied in organ chambers. α-Adrenoceptor agonists (norepinephrine, methoxamine, and UK14304) and antagonists (phentolamine hydrochloride [INN: phentolamine], prazosin, and yohimbine) were used to characterize the α-adrenoceptor. β-Adrenoceptor function was studied in U46619-precontracted rings in response to isoproterenol (INN: isoprenaline). Results: Norepinephrine induced 6.9 ± 0.6 gm (80.6% ± 6.8% of the contraction by 100 mmol/L KCl), and this was almost fully inhibited by phentolamine hydrochloride (10 μmol/L, p < 0.0001). The contraction force induced by methoxamine (2.9 ± 0.8 gm) was abolished by 0.5 μmol/L prazosin (p = 0.017). The contraction force induced by UK14304 (1.7 ± 0.4 gm) was abolished by 1 μmol/L yohimbine. In contrast to the porcine coronary artery used as the control (fully relaxed to isoproterenol), radial artery rings did not have significant relaxation (1.1% ± 0.8%). Conclusions: The human radial artery is an α-adrenoceptor–dominant artery with little β-adrenoceptor function. The use of β-blockers will not likely evoke the spasm of the radial artery. Furthermore, the radial artery has a dominant α1-adrenoceptor function, but the postjunctional α2-adrenoceptor is also functional. Circulating catecholamines will mainly contract the human radial artery by activation of the α1-adrenoceptors and to a lesser extent also by α2-adrenoceptors. (J Thorac Cardiovasc Surg 1998;115:88054-41)

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From the Division of Cardiothoracic Surgery and Cardiovascular Research Laboratory, Grantham Hospital, Department of Surgery, University of Hong Kong, Hong Kong.

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This study was supported by a Hong Kong Research Grants Council Grant (338/048/0001), the University of Hong Kong Committee of Research and Conference Grants (337/048/0018, 335/048/0079), and University of Hong Kong Grants (014/048/9602, 344/048/0001).

Address for reprints: Professor Guo-Wei He, MD, PhD, Chair of Cardiothoracic Surgery, University of Hong Kong, Grantham Hospital, 125 Wong Chuk Hang Rd., Aberdeen, Hong Kong.

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