The initial perfusion pressure was 100 mm
Hg (mean arterial pressure minus venous
pressure). Elevating the venous pressure to
15 mm Hg reduced the perfusion pressure to
85 mm Hg. According to the equation relating
blood flow, perfusion pressure, and vascular
resistance (F = AP/R), flow would decrease by
15% with a 15% decrease in perfusion pressure
(assuming that resistance does not change).
However, in this case, flow decreased by 25%
indicating that resistance increased by 13.3%
(R = AP/F = 0.85/0.75). The metabolic theory
for autoregulation states that as perfusion pres-
sure and flow are reduced, an accumulation of
vasodilator metabolites decreases resistance
in an attempt to restore flow; however, resist-
ance did not decrease in this experiment. The
myogenic theory states that increased trans-
mural pressure causes vascular smooth muscle
to contract, thereby increasing resistance and
decreasing flow. Increasing venous pressure in
this experiment increased the transmural pres-
sure in arterioles, causing them to constrict and
increase their resistance. Therefore, increasing
venous pressure produces opposite and com-
peting responses between these two mecha-
nisms. Because vascular resistance increased
in this experiment, we can conclude that the
myogenic (vasoconstrictor) mechanism was
dominant over the metabolic (vasodilator)
mechanism. These results have been observed
experimentally in organs such as the intestine.
CASE 7-1
It is important to control arterial pressure in
patients with coronary artery disease because
hypertension increases ventricular afterload
and myocardial oxygen demand. However, it
is important to lower arterial pressure using
drugs that do not cause a reflex tachycar-
dia for two reasons. First, reflex tachycardia
(baroreceptor-mediated) increases myocardial
oxygen demand and offsets the beneficial effects
of reducing afterload (see Chapter 4). Second,
tachycardia further impairs coronary perfu-
sion because the duration of diastole relative
to systole decreases at elevated heart rates.
This reduces the time available for coronary
perfusion during diastole, which is the time
when the greatest amount of coronary perfu-
sion occurs. It is common in clinical practice to
give a drug such as a [3-blocker to a patient with
both coronary artery disease and hypertension
because it lowers arterial pressure and prevents
reflex tachycardia.
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Deussen A, Brand M, Pexa A, Weichsel J. Metabolic
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Hill MA, Meininger GA, Davis MJ, Laher I. Therapeutic
potential of pharmacologically targeting arteriolar myo-
genic tone. Trends Pharmacol Sei 2009;30:363-374.
Johnson PC. Autoregulation of blood flow. Circ Res
Joyner MJ, Halliwill JR. Sympathetic vasodilation in
human limbs. J Physiol 2000;526:471-480.
Kellogg DL. In vivo mechanisms of cutaneous vaso-
dilation and vasoconstriction in humans dur-
ing thermoregulatory challenges. J Appl Physiol
Lassen NA: Brain. In Johnson PC, ed. Peripheral
Circulation. New York: John Wiley & Sons, 1978.
Rhoades RA, Bell, DR. Medical Physiology: Principles
for Clinical Medicine. 3rd Ed. Philadelphia:
Lippincott Williams & Wilkins, 2009.
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