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73rd APS President (2000-2001)
Gerald F. DiBona
(b. 1939)
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
Göteborg, Göteborg, 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.
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