Author + information
- Received May 4, 1988
- Revision received June 16, 1988
- Accepted June 21, 1988
- Published online November 1, 1988.
- ↵∗Address for reprints: David W. Ferguson, MD, Cardiovascular Division, Department of Internal Medicine, University of Iowa Hospitals, Iowa City, Iowa 52242.
To further evaluate the reported interaction in animals and humans between cardiopulmonary baroreflexes and the somatic pressor reflex, studies were performed in 16 normal men using direct measurements of efferent sympathetic nerve activity to muscle (microneurography) during sustained isometric handgrip (30% maximal voluntary contraction). Forearm vasoconstrictor (plethysmography) and muscle sympathetic nerve activity responses to sustained handgrip were measured during cardiopulmonary baroreceptor deactivation (lower body negative pressure, n = 8) and activation (volume expansion, n = 8). In addition, responses to posthandgrip muscle ischemia were studied during these perturbations of cardiopulmonary baroreflexes.
No evidence of an interaction between these two reflex pathways was found. When handgrip was performed during lower body negative pressure, the percent increase in muscle sympathetic nerve activity (+115 ± 17%) was not different fron the sum of the individual sympathetic responses to handgrip and lower body negative pressure performed separately (+106 ± 19%, p = NS). Likewise, the change in forearm vascular resistance (+3.9 ± 0.8 U) for sustained handgrip performed during lower body negative pressure was not different from the algebraic sum of the responses to handgrip and lower body negative pressure when these were performed separately (+4.7 ± 2.7 U, p = NS). No difference was noted in forearm vasoconstrictor and sympathetic nerve activity responses to posthandgrip muscle ischemia and lower body negative pressure when these were performed alone or in combination.
Volume expansion also failed to uncover an inhibitory interaction. Handgrip performed before volume expansion resulted in forearm vascular resistance responses (−1.2 ± 0.9 U) that were not different from the responses when such handgrip was performed after volume infusion (+0.9 ± 0.9 U, p = NS). Rather than producing the predicted inhibition of muscle sympathetic nerve activity responses to sustained handgrip, volume infusion actually increased these responses. During prevolume sustained handgrip, the increase in sympathetic nerve activity (+64.5 ± 15.7%) was significantly less than the increase when handgrip was performed after volume infusion (+105.6 ± 20.1%, p < 0.01). A similar lack of inhibitory modulation was seen during posthandgrip muscle ischemia performed before and after volume expansion. These data indicate that the efferent sympathetic responses to the somatic pressor reflex are not modulated by the cardiopulmonary baroreflexes in normal humans.
↵1 Dr. Ferguson is the recipient of a National institutes of Health New Investigator Award (1987 to 1990).
☆ This study was supported by Grants HL-39340 and HL-36224 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; a grant-in-aid from the Iowa Affiliate, American Heart Association, Iowa City, Iowa and General Clinical Research Grant RR-59, National Institutes of Health, Belhesda.
- Received May 4, 1988.
- Revision received June 16, 1988.
- Accepted June 21, 1988.