Vessel Wall - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 376

molecule of glucose, whereas mitochondrial glucose oxidation produce 36 mol of
ATP per molecule of glucose. Aerobic glycolysis has an advantage, as compartmen-
tation between the cytoplasm and mitochondria in ATP production is associated with
ion channel functioning and SMC excitability. There is also a compartmentation
of glucose metabolism in vascular smooth myocytes. Most exogenous glucose is
consumed in glycolysis and produced lactate, avoiding mitochondrial oxidation,
whereas in constricted cells intrinsic glucose released by glycogenolysis is oxidized
in mitochondria to fit the ATP demand during contraction. Acute hypoxia increases
mitochondrial and cytoplasmic NAD(P)H, but has opposite effects on mitochondria
and cytoplasmic redox systems [ 699 ]. Mitochondrial and cytoplasmic generation of
reactive oxygen species is augmented and lowered, respectively.
During hypoxia, oxygen-supplying pulmonary and placental arteries constrict,
whereas systemic arteries for oxygen-consuming organ perfusion dilate to achieving
optimal oxygen supply. Difference in mitochondrial features between vascular
smooth myocytes of pulmonary and systemic arteries could explain this opposed
behavior. Mitochondria of renal artery smooth myocytes are more hyperpolarized
than those of pulmonary artery smooth myocytes. Compartmentation between the
cytoplasm and mitochondria and difference in magnitude of metabolic enzyme
activity in both compartments between pulmonary and systemic arteries could
explain such a discrepancy.

7.11 Wall Adaptability

Proliferation of smooth myocytes can be modulated by growth factors and other
mediators, released from endothelial cells. Endothelial platelet-derived growth
factor-A that acts synergistically with endothelin-1, transforming growth factor- ,

and nitric oxide are secreted by endothelial cells, the secretion level depending on
flow conditions.
Angiotensin-2, formed by angiotensin-converting enzyme in a flow-dependent
manner, is a growth factor for vascular smooth muscle cells. Both serotonin and
thromboxane-A2, released by endothelial cells, or aggregating platelets at sites
of vascular injury, have a mitogenic effect from a given concentration via their
respective specific receptors [ 700 ]. These substances can synergistically interact;
SMC proliferation occurs at subthreshold concentrations.
Endothelium is able to adapt to ischemia. Nitric oxide contributes to car-
diomyocyte “hibernation” by reducing oxygen consumption and preserving calcium
sensitivity and contractile function without an energy cost during ischemia [ 701 ].
Hypoxemia induces the production of PGe2 and LTc4 by cardiomyocytes. Delayed
increase in NO production by NOS3 is a mediator of endothelial preconditioning,
with brief periods of ischemia-reperfusion that induce delayed protection of coro-
nary endothelial cells against reperfusion injury (ischemic preconditioning) [ 702 ].

β