316
6 Growth
6.11.1 Fundamental Adaptive Behavior of Arteries
The following paragraphs present some fundamental aspects of vascular adaptation.
It is important to keep in mind that regulation of pressure and flow often involves
features not considered here, including neural and hormonal factors (Berne and
Levy 1981).
Response to Pressure Perturbation Certain drugs and physiological conditions
can cause a sudden increase in blood pressure that increases vessel radius and wall
stress. The change in radius decreases vascular resistance by (6.117) and, therefore,
increases flow. Vascular smooth muscle responds to the sudden stretch by contracting, a phenomenon known as the myogenic response or Bayliss phenomenon, which
tends to restore the initial radius and flow (Berne and Levy 1981; Fung 1997). It
also decreases wall stress by (6.116).
For example, if Fred suddenly stands after spending all day lying down (as
usual), blood pools in his legs, depriving his brain of the oxygen needed to keep
it functioning at its normal extraordinary level. Responding to the sudden stretch,
arterioles constrict to decrease flow to his legs, leaving more blood for the brain and
other vital organs. In contrast, a partial occlusion or spasm in an artery can cause a
sudden decrease in blood pressure and flow downstream. The sudden pressure drop
causes smooth muscle in the downstream vessels to relax, increasing vascular radius
and flow.
As in the heart, chronic changes in pressure trigger a growth response in arteries,
with the wall growing thicker for elevated pressure and thinner for decreased
pressure to restore the homeostatic wall stress σ (Fig. 6.23a) (Taber 1995). As the
wall thickens during hypertension (high blood pressure), its collagen content also
increases (see next chapter). Both processes stiffen the wall, allowing the artery
to maintain a smaller radius without needing to maintain the elevated, energyconsuming contractile state. As the wall grows and remodels, normal tone is
reestablished.
Response to Flow Perturbation Increased oxygen demand in the tissues requires
increased blood flow into the capillaries, where gas exchange occurs. To increase
flow, arterioles open wider to decrease flow resistance; if demand drops, the lumen
diameter decreases to increase resistance. To a lesser extent, large arteries also can
contribute to a systemic change in flow resistance.
During the acute phase, these changes in geometry are again produced by
contraction and relaxation of smooth muscle, followed by growth and remodeling
during the chronic phase. However, whereas the response to a change in pressure
is regulated by circumferential wall stress σ , fluid shear stress τ controls the
response to a change in flow. Experiments have shown that an increase (decrease)
in flow rate triggers an increase (decrease) in radius that, via Eq. (6.118), returns
τ to its homeostatic value (Fig. 6.23b) (Kamiya and Togawa 1980). Interestingly,
measurements have indicated that τ is nearly the same in all arteries of a given
species (Kamiya and Togawa 1980; Kamiya et al. 1984).
6 Growth
6.11.1 Fundamental Adaptive Behavior of Arteries
The following paragraphs present some fundamental aspects of vascular adaptation.
It is important to keep in mind that regulation of pressure and flow often involves
features not considered here, including neural and hormonal factors (Berne and
Levy 1981).
Response to Pressure Perturbation Certain drugs and physiological conditions
can cause a sudden increase in blood pressure that increases vessel radius and wall
stress. The change in radius decreases vascular resistance by (6.117) and, therefore,
increases flow. Vascular smooth muscle responds to the sudden stretch by contracting, a phenomenon known as the myogenic response or Bayliss phenomenon, which
tends to restore the initial radius and flow (Berne and Levy 1981; Fung 1997). It
also decreases wall stress by (6.116).
For example, if Fred suddenly stands after spending all day lying down (as
usual), blood pools in his legs, depriving his brain of the oxygen needed to keep
it functioning at its normal extraordinary level. Responding to the sudden stretch,
arterioles constrict to decrease flow to his legs, leaving more blood for the brain and
other vital organs. In contrast, a partial occlusion or spasm in an artery can cause a
sudden decrease in blood pressure and flow downstream. The sudden pressure drop
causes smooth muscle in the downstream vessels to relax, increasing vascular radius
and flow.
As in the heart, chronic changes in pressure trigger a growth response in arteries,
with the wall growing thicker for elevated pressure and thinner for decreased
pressure to restore the homeostatic wall stress σ (Fig. 6.23a) (Taber 1995). As the
wall thickens during hypertension (high blood pressure), its collagen content also
increases (see next chapter). Both processes stiffen the wall, allowing the artery
to maintain a smaller radius without needing to maintain the elevated, energyconsuming contractile state. As the wall grows and remodels, normal tone is
reestablished.
Response to Flow Perturbation Increased oxygen demand in the tissues requires
increased blood flow into the capillaries, where gas exchange occurs. To increase
flow, arterioles open wider to decrease flow resistance; if demand drops, the lumen
diameter decreases to increase resistance. To a lesser extent, large arteries also can
contribute to a systemic change in flow resistance.
During the acute phase, these changes in geometry are again produced by
contraction and relaxation of smooth muscle, followed by growth and remodeling
during the chronic phase. However, whereas the response to a change in pressure
is regulated by circumferential wall stress σ , fluid shear stress τ controls the
response to a change in flow. Experiments have shown that an increase (decrease)
in flow rate triggers an increase (decrease) in radius that, via Eq. (6.118), returns
τ to its homeostatic value (Fig. 6.23b) (Kamiya and Togawa 1980). Interestingly,
measurements have indicated that τ is nearly the same in all arteries of a given
species (Kamiya and Togawa 1980; Kamiya et al. 1984).