Interaction of cardiopulmonary and carotid baroreflex control of vascular resistance in humans.

Abstract

IntroductionPrevious 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 < 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 Hypotension and hypovolemia often occur together in the clinical setting, so the arterial and cardiopulmonary baroreceptors are affected simultaneously (1). In most experimental studies of arterial and cardiopulmonary baroreflexes in humans, however, the reflexes have been activated individually, and the possibility of reflex interaction has received little attention (2). In contrast, an important interaction between high and low pressure baroreceptor reflexes has been demonstrated repeatedly in experimental animals (3-12). In the dog, for example, interruption of cardiopulmonary vagal afferents augments vasoconstrictor responses to carotid hypotension ( 12).Baroreflex interactions are obviously more difficult to study in human subjects than in experimental animals. In previous human studies ofthis reflex interaction, cardiopulmonary baroreflexes have been perturbed with lower body negative pressure (LBNP)' and carotid baroreflexes with neck suction. Using these methods, earlier experiments in this laboratory demonstrated that physiologic variations in central venous pressure do not alter carotid baroreflex control of heart rate in humans (13). Previous studies have also examined vascular responses during combined application of LBNP at -40 mmHg and neck suction (14-16). Because LBNP at -4...

Baroreceptor sensitivity in prehypertensive young adults.

“…22 LBNP at -10 mm Hg has been shown to decrease central venous pressure and cause forearm vasoconstriction without altering blood pressure or heart rate. 23 In the present study, systolic blood pressure decreased slightly at the lowest level of LBNP; however, blood pres-sure was not further reduced by increasing levels of LBNP. Heart rate, total peripheral resistance, and plasma norepinephrine concentrations increased progressively in response to graded levels of LBNP, and these responses did not differ in the high and low blood pressure groups.…”

The effect of sets and repetitions of the spirometer by flow in cardiorespiratory parameters

“…It has been reported that the interaction of the cardiopulmonary control and carotid baroreflex of the vascular resistance, which in directly related to the respiratory control and blood pressure, is due to the neurocirculatory adjustments for compensation that were changed in large by simultaneous alterations in the cardiopulmonary vagal afferent firing (23). The mean RR in the studied sample is consistent with the expected normal standards (12 to 20 rpm) and, even if the RR is normal, the increase in pulmonary ventilation by the incentive spiromenter consequently also provides RR reduction.…”

Arterial blood pressure response to head-up tilt test and orthostatic tolerance in nurses

“…The prolonged BP elevation is otherwise explained by a compensatory mechanism other than the arterial baroreflex, such as the cardiopulmonary baroreflex [6,7] or vestibulosympathetic reflex [8]. It is generally accepted that, in a prolonged stage ([2 min) of orthostasis, BP maintenance is supported by humoral factors [4,5].…”

“…However, the physiological implications of the lower BRS during HUT are unclear. One plausible explanation is that the reduced BRS during HUT resulted from an interaction of the arterial baroreflex with the cardiopulmonary baroreflex [6]. Furthermore, the reduction in BRS appears to contribute at least in part to the BP elevation during HUT, because it diminishes the buffering effect of the baroreflex on BP, and thereby allowing the BP to greatly fluctuate [44].…”

“…This blood shift then reduces the venous return, so that the cardiac output and blood pressure (BP) tend to decline. This BP reduction, however, is compensated partly by various reflex mechanisms including arterial baroreflex [4,5], cardiopulmonary reflex [6,7], vestibulosympathetic reflex [8], or venoarteriolar axon reflex [9], and thus BP is maintained during an upright posture. Improvement in orthostatic tolerance is achieved by improving orthostatic cardiovascular responses [10].…”