Abstract

Stimulation of left atrial volume receptors in the dog suppresses arginine vasopressin (AVP) release. Whether the same mechanism is valid in nonhuman primates and in humans is unclear. In order to investigate whether changes in low-pressure baroreceptor stimulation influence AVP release in humans, we utilized different experimental models (water immersion, lower body positive and negative pressure, and negative pressure breathing) to induce systematic changes in central venous pressure. In an additional study, carotid baroreceptors were selectively stimulated by neck suction in order to evaluate the role of arterial baroreceptors on AVP regulation. The results from these studies indicate that low-pressure baroreflexes play little or no role in the regulation of AVP release in overnight fluid-restricted humans during isoosmotic changes in central blood volume. It is suggested that high-pressure baroreflexes (probably in concert with other mechanisms) during these circumstances play a more important role and that changes in arterial pulse pressure (PP) and in the PP profile over time (dP/dt) may be more essential than changes in mean arterial pressure in regard to modulation of AVP release in humans. Future studies should focus on the effects of changes in arterial baroreceptor stimulation on AVP release in humans. In this regard, water immersion and selective carotid baroreceptor stimulation by neck suction are promising models.

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