Kenneth Byron, PhD
Title/s: <p> Professor Emeritus</p> <p>Molecular Pharmacology and Neuroscience</p> <p>Cell and Molecular Physiology</p>
Email: kbyron@luc.edu
Title/s: <p> Professor Emeritus</p> <p>Molecular Pharmacology and Neuroscience</p> <p>Cell and Molecular Physiology</p>
Email: kbyron@luc.edu
Research in the Byron lab is broadly related to the cellular and biochemical mechanisms that operate to regulate smooth muscle contraction. Smooth muscle is found in many tissues, including the walls of arteries (vascular smooth muscle) and the airways of the lung (airway smooth muscle). In arteries, the ability of smooth muscle cells to contract or relax allows for moment-to-moment control of artery diameter, and hence determines blood flow and blood pressure. A main objective of the research is to elucidate the molecular mechanisms by which vasoactive substances exert their effects, with a long-term goal of identifying improved therapeutic strategies for treatment of cardiovascular diseases. Research from this laboratory over the past 20 years has revealed novel cellular mechanisms that are activated by vasoconstrictor hormones, such as the pituitary hormone arginine vasopressin (AVP). The vasoconstrictor effects of AVP were found to involve inhibition of a specific class of potassium channels that were recognized as drug target in the nervous system. This research has helped explain off-target cardiovascular effects of the drugs when used to treat neurological conditions, and also suggested potential new uses of these drugs to treat cardiovascular conditions. One example of the latter is cerebral vasospasm, a devastating form of stroke that occurs following rupture of a cerebral aneurysm. Dr. Byron’s laboratory is collaborating with Loyola neurosurgeons and neurologists to design a clinical trial to test novel therapies for cerebral vasospasm based on their research on AVP vasoconstrictor mechanisms. In the airways of the lung, smooth muscle contraction can lead to narrowing of the airways, which can become excessive in conditions like asthma, resulting in obstruction of airflow. The Byron lab has found that the same proteins that are targeted by AVP in the vasculature are mediators of bronchoconstrictor actions that increase airway smooth muscle contraction in the lung. Ongoing research is investigating the molecular mechanisms by which airway smooth muscle ion channels contribute to bronchoconstrictor signal transduction, and determining how drugs that target potassium channels in airway smooth muscle might be more effective than currently used drugs in the relief of airflow obstruction in asthma and other airway diseases. In collaboration with clinical pulmonologists at Loyola, Dr. Byron and colleagues are designing a clinical trial to test the efficacy of drugs that target these mechanisms for relief of excessive airway smooth muscle contraction in patients with asthma.