Although the kidneys play a dominant role in restoring blood pressure to normal values over the long term, there are other blood volume-related mechanisms that can contribute to arterial pressure regulation. Two notable mechanisms that become activated within minutes to hours after a pressure change and whose effects can last for days are (1) the capillary fluid shift mechanism and (2) the stressrelaxation mechanism. The former mechanism involves a role for capillary hydrostatic pressure in promoting the filtration or absorption of fluid in the microvascu-lature during periods of high or low arterial pressure, respectively. Vascular beds that most likely contribute to this process include skeletal muscle and the splanchnic circulation. For example, if capillary pressure rises in response to increased blood volume or arterial pressure, then fluid will be filtered out of skeletal muscle capillaries at an accelerated rate. The resultant reduction in blood volume that occurs over hours will tend to restore arterial pressure and capillary pressure back toward their control values.
The stress-relaxation mechanism represents an effort by the blood vessels to fit around the existing blood volume. This phenomenon is related to the intrinsic ability of smooth muscle to return to its original force of contraction after it has been elongated or shortened. Stress-relaxation is more pronounced in the visceral smooth muscle surrounding hollow organs like the urinary bladder, but it does occur to some extent in vascular smooth muscle. Hence, if blood volume and arterial pressure become too high, the blood vessels are stretched and then slowly relaxed as though to accommodate a larger intravascular volume. As a result, the pressure within the arterial tree will fall toward normal. With hemorrhage, on the other hand, a reverse stressrelaxation will cause blood vessels to contract around the reduced blood volume, thereby tending to buffer the fall in arterial pressure.
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