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Ann Thorac Surg 2007;83:510-515
© 2007 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Regulation of Human Internal Mammary and Radial Artery Contraction by Extracellular and Intracellular Calcium Channels and Cyclic Adenosine 3', 5' Monophosphate

^a Department of Physiology, New York Medical College, Valhalla, New York
^b Department of Cardiothoracic Surgery, New York Medical College, Valhalla, New York

Accepted for publication September 1, 2006.

^_* Address correspondence to Dr Gupte, Department of Physiology, Room 626, Basic Sciences Building, New York Medical College, Valhalla, NY 10595. (Email: sachin_gupte{at}nymc.edu).

BACKGROUND: The internal mammary (IMA) and radial arteries (RA), which are routinely used in coronary artery bypass grafting, show a significant incidence of postoperative vasospasm. The present study evaluated the respective roles of calcium (Ca²⁺)–dependent and cyclic adenosine 3', 5' monophosphate–dependent (cAMP) signaling in mediating contraction and relaxation of the IMA and RA.

METHODS: We examined the contractile responses of the IMA and RA to potassium chloride, a depolarizing agent; phenylephrine, an -adrenergic agonist; and U46619, a thromboxane analogue, in the absence and presence (0.045 to 1.500 mM) of extracellular Ca²⁺.

RESULTS: Potassium chloride elicited little or no contraction in the absence of extracellular Ca²⁺. Contractions elicited by U46619 were similar in the IMA and RA, both in the absence and presence of extracellular Ca²⁺. By contrast, phenylephrine elicited significantly greater extracellular Ca²⁺-dependent contraction of the IMA than the RA. Estimation of cyclic guanosine 3', 5' monophosphate (cGMP) and cAMP revealed levels of cAMP to be about fourfold higher than cGMP in both the RA and IMA. Whereas forskolin and milrinone elicited similar relaxation of IMA and RA precontracted with either U46619 or phenylephrine and increased adenylate cyclase-catalyzed cAMP production, isoproterenol-induced relaxation of the arteries precontracted with U46619 was significantly impaired compared with arteries precontracted with phenylephrine.

CONCLUSIONS: Our findings suggest that thromboxane A₂ receptor–dependent pathways activate contraction of IMA and RA through both extracellular Ca²⁺-dependent and Ca²⁺-independent pathways. In addition, adenylate cyclase appears to play a key role in attenuating thromboxane A₂ and -adrenergic receptor-mediated contraction through both pathways.

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Invited commentary

Louis P. Perrault and Arnaud Mommerot
Ann. Thorac. Surg. 2007 83: 515-516. [Extract] [Full Text] [PDF]

This article has been cited by other articles:

				L. P. Perrault and A. Mommerot Invited commentary Ann. Thorac. Surg., February 1, 2007; 83(2): 515 - 516. [Full Text] [PDF]