Gerald F. DiBona
73rd APS President (2000-2001)
Gerald F. DiBona
Gerald DiBona is Professor and Vice Chairman of the Department of Internal Medicine at the University of Iowa College of Medicine in Iowa City, IA, where he has served since his appointment in 1969. Born in Cambridge, Massachusetts, he attended Harvard College, earning the AB in mathematics in 1960, and Tufts University School of Medicine, earning the MD cum laude in 1964. He received his clinical training in internal medicine at the Hospital of the University of Pennsylvania, Philadelphia from 1964-67. He returned to Boston for clinical and research training in nephrology and renal physiology at the Peter Bent Brigham Hospital and Harvard Medical School with John Merrill and Donald Oken from 1967-69. In 1969, he moved to the Department of Internal Medicine at the University of Iowa College of Medicine where he was appointed Assistant Professor in 1969, Associate Professor in 1972, and Professor in 1975. In 1977, he was appointed and continues to serve as Vice Chairman of the Department of Internal Medicine and Chief of the Medical Service, Iowa City Veterans Administration Medical Center. In 1997, he was appointed Professor, Department of Physiology and Biophysics, University of Iowa College of Medicine. In 2000, he was appointed Foreign Adjunct Professor, Karolinska Institute, Stockholm, Sweden.
During his nephrology fellowship, DiBona's research focused on renal micropuncture studies of the pathogenesis and recovery from experimental acute renal failure. After moving to Iowa, his research centered on the neural control of renal function. DiBona�s work demonstrated that the renal sympathetic nerves directly influence the function of each of the major renal effectors via direct and specific innervation. Intensities of renal sympathetic nerve stimulation that were subthreshold for effects on the renal vasculature or the juxtaglomerular apparatus directly increased renal tubular sodium and water reabsorption in multiple nephron segments without accompanying alterations in glomerular filtration rate, renal blood flow or hormonal release. This effect was shown to be mediated by a1-adrenoceptors located on the basolateral membrane of renal tubular epithelial cells whose stimulation increased basolateral sodium pump activity. The importance of this concept of low-intensity renal sympathetic nerve activity was expanded by the demonstration that during clinical conditions of increased renal sympathetic nerve activity and renal sodium retention (e.g., congestive heart failure), a substantial portion, circa 40%, of the excess renal sodium retention in these conditions was dependent on intact renal sympathetic innervation. Additional studies using measurements of single renal nerve fiber activity, analysis in the frequency domain and mathematical modeling of synchronized renal sympathetic nerve discharge have provided further evidence for the existence of functionally specific subgroups of renal sympathetic nerve fibers that are selectively targeted to the vessels, tubules or the juxtaglomerular granular cells.
Following a sabbatical period at the University of Göteborg, Göteborg, Sweden, DiBona incorporated the technique of recording renal sympathetic nerve activity in conscious animals to explore the interaction between the environmental factors, dietary salt intake and environmental stress, and genetic hereditary predisposition to the development of hypertension in the borderline hypertensive rat, a genetic salt-sensitive model of hypertension. An important finding was that dietary salt loading increased the renal sympathoexcitatory response to environmental stress resulting in further increased renal sodium retention and hypertension. Using cosegregation analysis in backcross populations, DiBona has identified quantitative trait loci for several aspects of the phenotype of abnormal regulation of renal sympathetic nerve activity in this model of genetic salt-sensitive model of hypertension.
Most recently, during a sabbatical period at Karolinska Institute, Stockholm, Sweden, DiBona has used laser confocal immunofluorescence microscopy in individual renal tubular epithelial cells to demonstrate that effects on the dynamics of receptor recycling may be a common underlying mechanism for the synergistic interaction between catecholamines (dopamine, norepinephrine) and neuropeptides (atrial natriuretic peptide, neuropeptide Y) that bind to G protein-coupled receptors.
DiBona has been an active member of APS since 1971, serving as Councillor for the Society for three years. He served as program representative for the Water & Electrolyte Homeostasis Section, as a member of the Publication Committee, and as Chair of the Committee on Committees. He has served on the editorial board of the American Journal of Physiology: Renal, Fluid and Electrolyte Physiology; American Journal of Physiology: Regulatory, Integrative and Comparative Physiology; and the American Journal of Physiology: Endocrinology & Metabolism. In addition to his service to APS, DiBona has served on scientific committees of FASEB, the American Society of Nephrology, the American Society of Hypertension, and the American Heart Association. He has served on scientific study sections for the VA, the American Heart Association, and the NIH, where he chaired the Cardiovascular and Renal Study Section. He served as founding Associate Editor for Journal of the American Society of Nephrology and Associate Editor and Editor-in-Chief for Hypertension. Currently, he is International Receiving Editor for Acta Physiologica Scandinavica and Clinical and Experimental Pharmacology and Physiology.
DiBona served as President of the American Federation for Clinical (now Medical) Research in 1979. He has received several awards: the Lewis K. Dahl Award from the Council for High Blood Pressure Research of the American Heart Association (1988), an Honorary Doctor of Medicine, University of G�teborg, G�teborg, Sweden (1993); the International Research Award of the International Society of Hypertension (1994); William S. Middleton Award for Outstanding Achievement in Biomedical or Behavioral Research of the Veterans Administration (1995); the Nobel Foundation Fellowship, Nobel Foundation, Stockholm, Sweden (1997-99); University of Iowa Regents Award for Faculty Excellence (1998); and Ernest H. Starling Distinguished Lectureship, Water & Electrolyte Homeostasis Section, American Physiological Society (2000). DiBona's research has been continuously funded by the National Institutes of Health since 1972 and the Veterans Administration since 1969.