Nonhypotensive lower body negative pressure produced a greater than twofold augmentation of the forearm vasoconstrictor response to neck pressure, demonstrating a specific inhibitory cardiopulmonary-carotid baroreflex interaction.
Does unloading of cardiopulmonary baroreceptors with nonhypotensive lower body negative pressure selectively augment reflex vasoconstrictor responses to simulated carotid hypotension in healthy humans?
Nonhypotensive lower body negative pressure selectively augments carotid baroreflex control of forearm vascular resistance, demonstrating a specific inhibitory cardiopulmonary-carotid baroreflex interaction in humans.
Absolute Event Rate: 38.2% vs 31.1%
p-value: p=<0.05
Previous studies in experimental animals indicate an important inhibitory interaction between cardiopulmonary and arterial baroreflexes. In the dog, for example, cardiopulmonary vagal afferents modulate carotid baroreflex control of vascular resistance. On the other hand, previous studies in human subjects have not produced convincing evidence of a specific interaction between these baroreceptor reflexes. The purpose of this study was to determine whether unloading of cardiopulmonary baroreceptors in humans with nonhypotensive lower body negative pressure selectively augments the reflex vasoconstrictor responses to simulated carotid hypotension produced by neck pressure. In nine healthy subjects, we measured forearm vascular responses with plethysmography during lower body negative pressure alone (cardiopulmonary baroreflex), during neck pressure alone (carotid baroreflex), and during concomitant lower body negative pressure and neck pressure (baroreflex interaction). Lower body negative pressure produced a greater than twofold augmentation of the forearm vasoconstrictor response to neck pressure. This increase in resistance was significantly greater (P less than 0.05) than the algebraic sum of the increase in resistance from lower body negative pressure alone plus that from neck pressure alone. In contrast, lower body negative pressure did not potentiate the forearm vasoconstrictor responses either to intra-arterial norepinephrine or to the cold pressor test. Thus, the potentiation of the vasoconstrictor response to neck pressure by lower body negative pressure cannot be explained by augmented reactivity to the neurotransmitter or to a nonspecific augmentation of responses to all reflex vasoconstrictor stimuli. In conclusion, nonhypotensive lower body negative pressure selectively augments carotid baroreflex control of forearm vascular resistance. These experiments demonstrate a specific inhibitory cardiopulmonary-carotid baroreflex interaction in humans.
Victor et al. (1985) studied Healthy (n=22). Concomitant lower body negative pressure and neck pressure vs. Lower body negative pressure alone or neck pressure alone was evaluated on Forearm vascular resistance (p=<0.05). Nonhypotensive lower body negative pressure produced a greater than twofold augmentation of the forearm vasoconstrictor response to neck pressure, demonstrating a specific inhibitory cardiopulmonary-carotid baroreflex interaction.