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J Thorac Cardiovasc Surg 2000;120:729-736
© 2000 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Contractile effects of arginine analogues on human internal thoracic and radial arteries

From the Departments of Physiology,^a Surgery,^b and Medicine,^c University of Valencia School of Medicine, Valencia, Spain.

Supported by the Comisión Interministerial de Ciencia y Tecnología, Ministerio de Sanidad and Generalitat Valenciana. G.S. was the recipient of a Fellowship of the Instituto de Salud Carlos III (99/9016).

Address for reprints: S. Lluch, MD, Departamento de Fisiología, Facultad de Medicina y Odontología, Blasco Ibáñez, 17, 46010 Valencia, Spain (E-mail: medinap{at}post.uv.es).

Objectives: Plasma levels of endogenous guanidino-substituted analogues of L-arginine are increased in various pathologic conditions. In the present study we determined the effects of some of these compounds on basal and stimulated release of nitric oxide in human internal thoracic and radial arteries.
Methods: Rings of human internal thoracic and radial arteries were obtained from 16 multiorgan donors. The rings were suspended in organ baths for isometric recording of tension.
Results: N^G-monomethyl L-arginine (10^–6 to 10^–3 mol/L) and N^G,N^G-dimethyl L-arginine (10^–6 to 10^–3 mol/L) caused concentration- and endothelium-dependent contractions. Maximal force of contractions for N^G-monomethyl L-arginine and N^G,N^G-dimethyl L-arginine in the internal thoracic artery were 18.0% ± 4.3% and 17.8% ± 3.8%, respectively, of the contraction to 100 mmol/L KCl, and those found in the radial artery were 9.6% ± 2.5% and 9.1% ± 2.4%, respectively. Aminoguanidine (10^–5 to 3 x 10^–3 mol/L) and methylguanidine (10^–5 to 3 x 10^–3 mol/L) produced endothelium-independent contractions. L-Arginine (10^–3 mol/L) prevented the contractions by N^G-monomethyl L-arginine and N^G,N^G-dimethyl L-arginine but did not change contractions induced by aminoguanidine and methylguanidine. N^G-monomethyl L-arginine and N^G,N^G-dimethyl L-arginine inhibited, in a concentration-dependent manner, the endothelium-dependent relaxation to acetylcholine in the internal thoracic artery and had little attenuating effect in the radial artery; aminoguanidine and methylguanidine were without effect.
Conclusions: The results suggest that the contractions induced by N^G-monomethyl L-arginine and N^G,N^G-dimethyl L-arginine are due to inhibition of both basal and stimulated nitric oxide production, whereas aminoguanidine and methylguanidine do not affect the synthesis of nitric oxide. An increase in the plasma concentration of N^G-monomethyl L-arginine and N^G,N^G-dimethyl L-arginine is likely to represent a risk factor for abnormal vasomotor tone in conduit arteries used as coronary grafts.