51st APS President (1978-1979)
David Francis Bohr
1915-2008
As president elect of APS, in the fall of 1977 Bohr visited medical
schools and especially departments of physiology in Cuba (11). He reported
that under Communist management the national rate of illiteracy has been
reduced from twenty-five percent to three percent; that the 3,000 physicians
who left Cuba after the revolution have been replaced threefold, resulting
in a current physician-to-population ratio higher than in the United States;
and that medical education is not only of good quality, but also is free,
with students receiving in addition an allowance for living expenses. He
found physiology to be an active profession in both teaching and research.
The president of the Cuban Physiological Society, F. R. Dorticos, seemed
interested in the possibility of joint meetings of his society and APS,
possibly in cooperation with the Mexican Physiological Society or with the
Latin American Society of Physiological Sciences. As a result of Bohr's
initiative, the Latin American society was invited to take part in the APS
Fall Meeting in San Diego in October 1982. There the president of the Latin
American society, Cesar Tim-Iaria of Sao Paulo, Brazil, met with Council to
discuss ways to foster better communication between the Americas.
Although for more than fifty years Bohr's career has been identified with
the University of Michigan, he was born in Zurich, Switzerland, lived for
five years as a boy in Cuba, and received most of his primary school
education in the southernmost part of California. In 1933 he entered the
University of Michigan, matriculated in 1936 in its medical school, and
graduated in 1942 after having spent two years as a teaching and research
assistant in the Department of Physiology where Robert Gesell was chairman.
Bohr interned at Henry Ford Hospital for a year before he was assigned by
the U.S. Army to a Dutch hospital ship for three years of duty as laboratory
officer and detachment commander (1943-46). He then spent two years
(1946-48) as a research fellow at the University of California in San
Francisco before returning permanently to the University of Michigan. In
1957 he was promoted to the rank of professor.
On two occasions Bohr has served as visiting professor, first in 1955-56
at the Department of Pharmacology at the University of California at San
Francisco and again in 1961-62 at the Physiologische Institut at Heidelberg.
Michigan chose him for a Distinguished Faculty Achievement Award in 1973 and
for the Distinguished Faculty Lectureship in Biological Research in 1983. In
1977 he gave the Wiggers Lecture for APS, and in 1984 he received the Ciba
Award for Hypertension Research. He is a member of the International Society
of Hypertension, the InterAmerican Hypertension Society, and the Council for
High Blood Pressure Research of AHA (1968-; chairman, 1978-80). For five
years (1969-74) he was a member of the Research Advisory Committee of AHA
and also chairman of one of its cardiovascular study committees.
As a member of the Physiology Study Section, Bohr began association with
NIH advisory groups in 1960-64. He served with the NIH Hypertension Task
Force (1978-79) and on the Study Section B of the Heart, Lung and Blood
Institute (1981-86). He has been a member of the Committee on Physiology of
the National Board of Medical Examiners (1965-68) and also of the
Cardiovascular Review Panel for the Space Science Board of NAS (1968-72).
Most of his editorial responsibilities have similarly involved the
circulatory system. He served the Society on the Editorial Board of its
journals in 1966-69, in 1969-75 as coeditor of the circulation section of
the American Journal of Physiology, and in 1983-86 as associate
editor of the American Journal of Physiology: Heart and Circulatory
Physiology. He also served as editor of the Handbook of Physiology,
Vascular Smooth Muscle. He was a member of the editorial boards of
Circulation Research (1960-65 and 1968-74), Proceedings of the
Society for Experimental Biology and Medicine (1978-81), Blood
Vessels (1974-), and Hypertension (1979-81).
Bohr joined APS in 1949. His earliest committee responsibility was with
the Membership Committee (1966-69; chairman, 1967-69). for a year (1969-70)
he was chairman of the Subcommittee on Undergraduate Education in Physiology
and then joined the Education Committee (1970-73). In 1970-73 he was a
member of the Steering Committee of the Circulation Group of the Society.
From 1974-1977 he served with the Perkins Memorial Fund Committee, after his
election to Council in 1973. He became president elect in 1977. Regarding
his presidential years, Bohr has written:
"There are two things for which I feel some satisfaction during my tenure
at the helm. One was the institution of the Standing Committee on Career
Opportunities in Physiology. Walter Randall agreed to serve as first
chairman of the committee, and at least half of the members are to be under
the age of forty years. Anything we can do to help those who are getting
launched in our field will be of value to our profession and will be much
appreciated by those we are helping. The other memorable event was the
Society's support of my visit to Cuba (11). It initiated a regrettably
abortive relationship with physiologists in Cuba, which I certainly would
like to see rekindled. It will not be easy, but I would be glad to help."
A third important event was a meeting Bohr encouraged between members of
the APS Animal Care Committee and representatives of animal welfare groups.
In February 1980, Helene Cecil, chairwoman of the APS committee, met with
Leon Bernstein and Christine Stevens and others of the Animal Welfare
Institute for discussion of the use of animals and alternatives to such use
in research and teaching. Christine Stevens is the daughter of Bohr's
mentor, Robert Gesell. The meeting was reported briefly in The
Physiologist [23(3): 16, 1980].
In regard to his research interests, training, and publications, Bohr
wrote:
"[At first] I worked with John Bean in the Department of Physiology on
oxygen toxicity (1). It was obvious then and still is that you can get major
rewards in physiology from problem solving by using physical and chemical
tools plus common sense. . . . I then began to be interested primarily in
the contractile machinery of vascular smooth muscle, which made me want to
know what causes the pressure to go up in hypertension. I have been working
at these two problems for the last thirty years."
"It is an interesting coincidence that both of my favorite publications
appeared in Science. The first (2) demonstrated that calcium not only
causes contraction of vascular smooth muscle but also in higher
concentrations decreases excitability. The second, published two years later
(3), quantified the calcium requirement for contractile activity of vascular
smooth muscle and skeletal muscle and showed that the contractile apparatus
of the two machines has identical calcium dependency. Recently, I have been
trying to understand those changes in contractile machinery of resistance in
hypertension. . . . Here are thumbnail sketches of later papers."
Reference 4. Small coronary arteries from the dog have little or no
alpha-adrenergic activity but respond to catecholamines with relaxation
resulting from activation of beta-adrenergic receptors. Large coronary
arteries have both alpha- and beta-adrenergic activity. The beta-receptors
of coronary vessels appear to differ from those in vessels supplying
skeletal muscle.
Reference 5. There is an as yet unidentified vasoactor in plasma that
causes contraction of isolated vascular smooth muscle. This factor may play
a role in the maintenance of normal vascular tone.
Reference 6. Sensitivity of vascular smooth muscle to constrictor
agonists was found to be elevated in deoxycorticosterone acetate, renal, and
spontaneously hypertensive rats. This increase in sensitivity reflects a
lessening of calcium binding to the cell membrane in vascular smooth muscle
from rats with these types of hypertension.
Reference 7. The increase in sensitivity of vascular smooth muscle from
hypertensive rats was demonstrated to be primary. It occurred in the
hindlimb vasculature that was protected from the hypertension by ligation of
the iliac artery.
Reference 8. Vascular smooth muscle made to contract in a potassium-free
medium undergoes a relaxation when potassium is added back to the muscle
bath. This relaxation was demonstrated to be due to membrane
hyperpolarization resulting from activation of the electrogenic sodium pump.
this phenomenon was subsequently used extensively to evaluate sodium pump
activity in isolated vascular smooth muscle.
Reference 9. Pressor responses to intravenous infusions of norepinephrine
or of angiotensin were elevated as early as two days after the beginning of
treatment of the pig with deoxycorticosterone acetate.
Reference 10. Blood pressure elevation in the pig began two days
following deoxycorticosterone acetate treatment and reached a plateau three
weeks later. The pressure elevation was caused in some pigs by an elevation
in cardiac output and in others by an elevation in total peripheral
resistance, but in most animals it was caused by an elevation in both of
these determinants of arterial pressure.
Reference 13. Evidence is presented to support a hypothesis that the
primary fault in the pathophysiology of hypertension is a defect in the
calcium binding of the plasma membrane of the cells of a pressure-regulating
center in the hypothalamus.
Reference 14: Basilar arteries from spontaneously hypertensive rats (but
not from normotensive controls) were characterized by spontaneous
contraction which resulted form a membrane leak of extracelluar calcium.
Reference 15. Administration of deoxycorticosterone to the sheep results
in hypertension, polydipsia, hypokalemia, and the development of a "salt
appetite."
Reference 16. Treatment of isolated vascular smooth muscle with serotonin
results in the following sequence of events that causes an attenuation of
the response resulting from subsequent stimulation of the muscle with
norepinephrine: 1) increased membrane permeability to sodium, 2)
elevated intracellular sodium, 3) stimulation of the sodium efflux
pump, 4) membrane hyperpolarization, and 5) depressed calcium
influx via the norepinephrine-operated receptor.
One of the themes that occurs and recurs in past-presidential addresses
is the responsibility of physiologists in the overall enterprise of medical
education and perhaps in what is know as "delivery" of health care. Bohr
(12) pointed out that problems in medical practice have two parts: 1)
economy or finances and 2) attitude. After summarizing how medical
costs have become so high, he spoke of the contrast between what has
happened in the United States and what he observed in Cuba. There health
care is available to all without charge. Yet even though Cuban education and
health care have moved forward rapidly, any visitor can see that "the
economy is clearly an unsurmounted hurdle. Housing is poor, manufactured
items are in scarce supply, clothing is rationed, and very few people have
their own automobiles" (11). Later he added, "and besides, there is
virtually nothing to buy" (12).
Bohr ended his remarks with a few words about improving attitudes of
physicians and how medical education might be modified to preserve
throughout their training the sensitive, ethical dedication students bring
to medical school. "Sensitivity and feeling add nothing to the cost of
health care." As physiologists working within medical schools, because "we
train future clinical doctors, nurses, and dentists, we hold a measure of
responsibility for the caliber, the quality, and the integrity of health
care in America that we cannot disown."
Selected Publications
1. Bean, J. W., and D. F. Bohr.. High oxygen effects on isolated striated
muscle. Am. J. Physiol. 126: 188-195, 1939.
2. Bohr, D. F. Vascular smooth muscle: dual effect of calcium. Science
Wash. DC 139: 597-599, 1963.
3. Filo, R. S., D. F. Bohr, and J. C. Ruegg. Glycerinated skeletal and
smooth muscle: calcium and magnesium dependence. Science Wash. DC
147: 1581-1583, 1965.
4. Bohr, D. F. Adrenergic receptors in coronary arteries. Ann. NY
Acad. Sci. 139: 799-807, 1967.
5. Bohr, D. F., and J. Sobieski. A vasoactive factor in plasma.
Federation Proc. 27: 1396-1398, 1968.
6. Holloway, E. T., and D. F. Bohr. Reactivity of vascular smooth muscle
in hypertensive rats. Circ. Res. 33: 678-685, 1973.
7. Hansen, T. R., and D. F. Bohr. Hypertension, transmural pressure, and
vascular smooth muscle response in rats. Circ. Res. 36: 590-598,
1975.
8. Bonaccorsi, A., K. Hermsmeyer, O. Aprigliano, C. B. Smith, and D. F.
Bohr. Mechanism of potassium relaxation of arterial muscle. Blood Vessels
14: 261-276, 1977.
9. Berecek, K. H., and D. F. Bohr. Whole body vascular reactivity during
the development of deoxycorticosterone acetate hypertension in the pig.
Circ. Res. 42: 764-771, 1978.
10. Miller, A. W., D. F. Bohr, A. M. Schork, and J. M. Terris.
Hemodynamic responses to DOCA in young pigs. Hypertension Dallas 1:
591-597, 1979.
11. Bohr, D. F. President-elect's tour. Changes in Cuba. Physiologist
22(1): 9-11, 1979.
12. Bohr, D. F. Past-president's address. The health market and
physiologists. Physiologist 22(6): 15-17, 1979.
13. Bohr, D. F. What makes the pressure go up? A hypothesis.
Hypertension Dallas 3, Suppl. II: 160-165, 1981.
14. Winquist, R. J., and D. F. Bohr. Structural and functional changes in
cerebral arteries from spontaneously hypertensive rats. Hypertension
Dallas 5, Suppl. III: 292-297, 1983.
15. MItchell, J., W. D. Ling, and D. F. Bohr. Deoxycorticosterone acetate
hypertension in sheep. J. Hypertension 2: 473-478, 1984.
16. Moreland, R. S., C. van Breemen, and D. F. Bohr. Mechanism by which
serotonin attenuates contractile response of canine mesenteric arterial
smooth muscle. J. Pharmacol. Exp. Ther. 232: 322-329, 1985.
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