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Ann Thorac Surg 2000;70:2064-2069
© 2000 The Society of Thoracic Surgeons

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Original article: cardiovascular

Inhibition of vasoconstriction by angiotensin receptor antagonist GR117289C in arterial grafts

^a Cardiovascular Research, The Albert Starr Academic Center For Cardiac Surgery, Providence St. Vincent Hospital, Portland, Oregon, USA
^b Department of Surgery, The Chinese University of Hong Kong, Hong Kong SAR, China

Accepted for publication April 19, 2000.

Address reprint requests to Dr He, Division of Cardiothoracic Surgery, Department of Surgery, University of Hong Kong, 5A, Block B, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China
e-mail: gwhe{at}cuhk.edu.hk

Background. Angiotensin II (AII) has been suggested to be one of the important factors for genesis of graft spasm in coronary artery bypass surgery. The aim of this work was to investigate the effects of the nonpeptide angiotensin receptor AT₁ antagonist GR117289C on the contraction induced by AII and other vasoconstrictors in isolated human internal mammary artery (IMA) preparations.

Methods. Two hundred eight IMA rings taken from 64 patients undergoing coronary artery bypass grafting were studied in organ baths. The interaction between GR117289C and AII or the other vasoconstrictors (U46619, norepinephrine, endothelin-1, and potassium chloride) was investigated in two ways.

Results. GR117289C induced near-maximal relaxation (94.5% ± 2.9%) in IMA rings precontracted by AII. In IMA rings incubated with 1 or 10 nmol/L GR117289C, contractile responses to AII were attenuated in a concentration-related manner, whereas the dose-response curve did not shift to the right when higher doses of AII were administered, suggesting that the AT₁ receptor blockade was noncompetitive in nature. Moreover, GR117289C also induced significant relaxation (82.9% ± 8.1%) in IMA rings precontracted by U46619, but no inhibitory responses to U46619 could be observed when IMA rings were incubated with GR117289C. GR117289C did not alter responses to potassium chloride, norepinephrine, and endothelin-1.

Conclusions. These results indicate that GR117289C is a potent, selective, noncompetitive AT₁ receptor antagonist that may have a possible antagonistic effect on the thromboxane A₂ receptor. Because AII and thromboxane A₂ are important vasoconstrictors in the genesis of graft spasm, GR117289C may become an alternative treatment to relieve graft spasm.

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