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Coronary artery vasodilation is the physiological process by which the smooth muscle in coronary arteries relaxes to increase blood flow and supply oxygen to the myocardium according to demand. It is regulated primarily by local metabolic factors (such as adenosine and nitric oxide), autonomic signaling, and the actions of various ion channels (K+, Ca2+), receptors (adenosine types A1, A2A, A2B, etc.), and endothelial mediators. The process is fundamental in maintaining cardiac perfusion and responding to increased cardiac workload or ischemic conditions, and is a central therapeutic target for drugs used to treat angina and ischemic heart conditions. However, "coronary artery vasodilation" itself is a process, not a unique molecule or receptor, and should not be listed as a molecular target; instead, the underlying molecular mediators—such as adenosine A2A receptor, nitric oxide synthase, potassium channels—are appropriate molecular targets for drug development.
Activation of adenosine receptors (A2A subtype) leading to cAMP-mediated smooth muscle relaxation; Nitric oxide release and cGMP-mediated vasodilation; Blockade of calcium channels lowering intracellular Ca2+; Opening of potassium channels leading to membrane hyperpolarization and relaxation; Phosphodiesterase inhibition increasing cAMP and/or cGMP
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