Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans

Virend Somers, A. L. Mark, F. M. Abboud

Research output: Contribution to journalArticle

273 Citations (Scopus)

Abstract

Animal studies have demonstrated that activation of the baroreflex by increases in arterial pressure inhibits cardiovascular and ventilatory responses to activation of peripheral chemoreceptors (PC) with hypoxia. In this study, we examined the influences of baroreflex activation on the sympathetic response to stimulation of PC and central chemoreceptors in humans. PC were stimulated by hypoxia (10% O2/90% N2) (n = 6) and central chemoreceptors by hypercapnia (7% CO2/93% O2) (n = 6). Responses to a cold pressor stimulus were also obtained as an internal reflex control to determine the selectivity of the interactive influence of baroreflex activation. Baroreflex activation was achieved by raising mean blood pressure by > 10 mmHg with intravenous infusion of phenylephrine (PE). Sympathetic nerve activity (SNA) to muscle was recorded from a peroneal nerve (microneurography). During hypoxia alone, SNA increased from 255 ± 92 to 354 ± 107 U/min (P < 0.05). During PE alone, mean blood pressure increased and SNA decreased to 87 ± 45 U/min (P < 0.05). With hypoxia during baroreflex activation with PE, SNA did not increase (50 ± 23 U/min). During hypercapnia alone, SNA increased from 116 ± 39 to 234 ± 72 U/min (P < 0.01). Hypercapnia during baroreflex activation with PE increased SNA from 32 ± 25 U/min during PE alone to 61 ± 26 U/min during hypercapnia and PE (P < 0.05). Like hypercapnia (but unlike hypoxia) the cold pressor test also increased SNA during PE. We conclude that baroreflex activation selectively abolishes the SNA response to hypoxia but not to hypercapnia or the cold pressor test. The inhibitory interaction of the baroreflex and the peripheral chemoreflex may be explained by convergence of baroreceptor and peripheral chemoreceptor afferents on neurons in the medulla.

Original languageEnglish (US)
Pages (from-to)1953-1957
Number of pages5
JournalJournal of Clinical Investigation
Volume87
Issue number6
StatePublished - 1991
Externally publishedYes

Fingerprint

Baroreflex
Phenylephrine
Hypercapnia
Blood Pressure
Afferent Neurons
Peroneal Nerve
Pressoreceptors
Intravenous Infusions
Reflex
Hypoxia
Arterial Pressure
Muscles

Keywords

  • Baroreflex
  • Chemoreflex
  • Hypercapnia
  • Hypoxia

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans. / Somers, Virend; Mark, A. L.; Abboud, F. M.

In: Journal of Clinical Investigation, Vol. 87, No. 6, 1991, p. 1953-1957.

Research output: Contribution to journalArticle

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abstract = "Animal studies have demonstrated that activation of the baroreflex by increases in arterial pressure inhibits cardiovascular and ventilatory responses to activation of peripheral chemoreceptors (PC) with hypoxia. In this study, we examined the influences of baroreflex activation on the sympathetic response to stimulation of PC and central chemoreceptors in humans. PC were stimulated by hypoxia (10{\%} O2/90{\%} N2) (n = 6) and central chemoreceptors by hypercapnia (7{\%} CO2/93{\%} O2) (n = 6). Responses to a cold pressor stimulus were also obtained as an internal reflex control to determine the selectivity of the interactive influence of baroreflex activation. Baroreflex activation was achieved by raising mean blood pressure by > 10 mmHg with intravenous infusion of phenylephrine (PE). Sympathetic nerve activity (SNA) to muscle was recorded from a peroneal nerve (microneurography). During hypoxia alone, SNA increased from 255 ± 92 to 354 ± 107 U/min (P < 0.05). During PE alone, mean blood pressure increased and SNA decreased to 87 ± 45 U/min (P < 0.05). With hypoxia during baroreflex activation with PE, SNA did not increase (50 ± 23 U/min). During hypercapnia alone, SNA increased from 116 ± 39 to 234 ± 72 U/min (P < 0.01). Hypercapnia during baroreflex activation with PE increased SNA from 32 ± 25 U/min during PE alone to 61 ± 26 U/min during hypercapnia and PE (P < 0.05). Like hypercapnia (but unlike hypoxia) the cold pressor test also increased SNA during PE. We conclude that baroreflex activation selectively abolishes the SNA response to hypoxia but not to hypercapnia or the cold pressor test. The inhibitory interaction of the baroreflex and the peripheral chemoreflex may be explained by convergence of baroreceptor and peripheral chemoreceptor afferents on neurons in the medulla.",
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