Acute non-hypotensive hemorrhage of 10-20% blood volume sharply reduced atrial stretch receptor firing and significantly increased blood ADH levels in conscious animals.
Does non-hypotensive hemorrhage affect atrial stretch receptor firing and ADH release in conscious animals?
Non-hypotensive hemorrhage reduces atrial stretch receptor firing and increases ADH release, highlighting the role of the low-pressure system in fluid volume regulation.
Moderate hemorrhage insufficient to reduce seriously the pulse pressure, had no effect on the total flow of afferent impulses per unit time from stretch receptors of the high-pressure system (systemic circulation). However, it sharply reduced the flow from the atrial receptors of the low-pressure system (lesser circulation). Thus acute non-hypotensive blood volume loss permits a differentiation between the effects of the stretch receptors in the two divisions of the cardiovascular system. Eleven conscious animals were trained to lie quietly with catheters in the femoral vessels. The loss of no more than 10–20% of the estimated blood volume led to a sharp drop in atrial stretch receptor firing. Measurements of blood ADH showed variable increases which in most cases were to significant levels. Other aspects of cardiovascular and fluid volume regulation were affected by changes in firing of stretch receptors in the low-pressure system. They include the tachycardia of non-hypotensive hemorrhage and changes in kidney function with atrial distension.
Henry et al. (1968) studied Non-hypotensive hemorrhage (n=11). Acute non-hypotensive hemorrhage was evaluated on Atrial stretch receptor firing and blood ADH levels. Acute non-hypotensive hemorrhage of 10-20% blood volume sharply reduced atrial stretch receptor firing and significantly increased blood ADH levels in conscious animals.