Central interaction between carotid baroreceptors and skeletal muscle receptors inhibits sympathoexcitation

Jeffrey T. Potts, Gregory A. Hand, Jianhua Li, Jere H. Mitchell

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

To determine the potential of an inhibitory interaction between the carotid sinus baroreflex (CSB) and the exercise pressor reflex (EPR), both pathways were activated to produce sympathoexcitation. It was hypothesized that, under conditions when the baroreflex increased sympathetic outflow, the interaction between CSB and EPR would be inhibitory. Bilateral carotid occlusion (BCO), electrically induced muscle contraction (EMC), and passive muscle stretch (PMS) were used to evoke sympathoexcitation. BCO decreased sinus pressure 50 ± 5 mmHg, and the levels of muscle tension generated by EMC and PMS were 7 ± 2 and 8 ± 1 kg, respectively. This resulted in significant increases in mean arterial pressure (MAP) of 55 ± 9, 50 ± 7, and 50 ± 6 mmHg (P = not significant, BCO vs. EMC vs. PMS) and in heart rate (HR) of 7 ± 2, 19 ± 4, and 17 ± 2 beats/min (P < 0.05, BCO vs. EMC and PMS). When BCO was combined with EMC or PMS, the reflex increase in MAP was augmented (80 ± 8 and 79 ± 10 mmHg; BCO+EMC and BCO+PMS, respectively; P < 0.05). However, summation of the individual MAP responses was greater than the response evoked during coactivation (106 ± 11 and 103 ± 12 mmHg, respectively, P < 0.05). Because summing the individual blood pressure responses exceeded the response during coactivation, the net effect was that the CSB and EPR interacted in an occlusive manner. In contrast, summation of the individual chronotropic responses was the same as the response evoked during coactivation. Moreover, there was no difference in summation of the individual MAP or HR responses when muscle afferents were activated by either EMC or PMS. In conclusion, the interaction between the CSB and the EPR in control of MAP was occlusive when both reflexes were stimulated to evoke sympathoexcitation. However, summation of the reflex changes in HR was simply additive.

Original languageEnglish (US)
Pages (from-to)1158-1165
Number of pages8
JournalJournal of Applied Physiology
Volume84
Issue number4
StatePublished - Apr 1998

Fingerprint

Pressoreceptors
Muscle Contraction
Skeletal Muscle
Baroreflex
Reflex
Muscles
Carotid Sinus
Arterial Pressure
Heart Rate
Stretch Reflex
Muscle Tonus
Blood Pressure
Pressure

Keywords

  • Baroreceptor afferents
  • Blood pressure
  • Exercise
  • Heart rate
  • Somatic afferents
  • Static muscle contraction
  • Sympathetic nerve activity

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Central interaction between carotid baroreceptors and skeletal muscle receptors inhibits sympathoexcitation. / Potts, Jeffrey T.; Hand, Gregory A.; Li, Jianhua; Mitchell, Jere H.

In: Journal of Applied Physiology, Vol. 84, No. 4, 04.1998, p. 1158-1165.

Research output: Contribution to journalArticle

@article{e1b03509eaa940959682b682f499adb8,
title = "Central interaction between carotid baroreceptors and skeletal muscle receptors inhibits sympathoexcitation",
abstract = "To determine the potential of an inhibitory interaction between the carotid sinus baroreflex (CSB) and the exercise pressor reflex (EPR), both pathways were activated to produce sympathoexcitation. It was hypothesized that, under conditions when the baroreflex increased sympathetic outflow, the interaction between CSB and EPR would be inhibitory. Bilateral carotid occlusion (BCO), electrically induced muscle contraction (EMC), and passive muscle stretch (PMS) were used to evoke sympathoexcitation. BCO decreased sinus pressure 50 ± 5 mmHg, and the levels of muscle tension generated by EMC and PMS were 7 ± 2 and 8 ± 1 kg, respectively. This resulted in significant increases in mean arterial pressure (MAP) of 55 ± 9, 50 ± 7, and 50 ± 6 mmHg (P = not significant, BCO vs. EMC vs. PMS) and in heart rate (HR) of 7 ± 2, 19 ± 4, and 17 ± 2 beats/min (P < 0.05, BCO vs. EMC and PMS). When BCO was combined with EMC or PMS, the reflex increase in MAP was augmented (80 ± 8 and 79 ± 10 mmHg; BCO+EMC and BCO+PMS, respectively; P < 0.05). However, summation of the individual MAP responses was greater than the response evoked during coactivation (106 ± 11 and 103 ± 12 mmHg, respectively, P < 0.05). Because summing the individual blood pressure responses exceeded the response during coactivation, the net effect was that the CSB and EPR interacted in an occlusive manner. In contrast, summation of the individual chronotropic responses was the same as the response evoked during coactivation. Moreover, there was no difference in summation of the individual MAP or HR responses when muscle afferents were activated by either EMC or PMS. In conclusion, the interaction between the CSB and the EPR in control of MAP was occlusive when both reflexes were stimulated to evoke sympathoexcitation. However, summation of the reflex changes in HR was simply additive.",
keywords = "Baroreceptor afferents, Blood pressure, Exercise, Heart rate, Somatic afferents, Static muscle contraction, Sympathetic nerve activity",
author = "Potts, {Jeffrey T.} and Hand, {Gregory A.} and Jianhua Li and Mitchell, {Jere H.}",
year = "1998",
month = "4",
language = "English (US)",
volume = "84",
pages = "1158--1165",
journal = "Journal of Applied Physiology",
issn = "0161-7567",
publisher = "American Physiological Society",
number = "4",

}

TY - JOUR

T1 - Central interaction between carotid baroreceptors and skeletal muscle receptors inhibits sympathoexcitation

AU - Potts, Jeffrey T.

AU - Hand, Gregory A.

AU - Li, Jianhua

AU - Mitchell, Jere H.

PY - 1998/4

Y1 - 1998/4

N2 - To determine the potential of an inhibitory interaction between the carotid sinus baroreflex (CSB) and the exercise pressor reflex (EPR), both pathways were activated to produce sympathoexcitation. It was hypothesized that, under conditions when the baroreflex increased sympathetic outflow, the interaction between CSB and EPR would be inhibitory. Bilateral carotid occlusion (BCO), electrically induced muscle contraction (EMC), and passive muscle stretch (PMS) were used to evoke sympathoexcitation. BCO decreased sinus pressure 50 ± 5 mmHg, and the levels of muscle tension generated by EMC and PMS were 7 ± 2 and 8 ± 1 kg, respectively. This resulted in significant increases in mean arterial pressure (MAP) of 55 ± 9, 50 ± 7, and 50 ± 6 mmHg (P = not significant, BCO vs. EMC vs. PMS) and in heart rate (HR) of 7 ± 2, 19 ± 4, and 17 ± 2 beats/min (P < 0.05, BCO vs. EMC and PMS). When BCO was combined with EMC or PMS, the reflex increase in MAP was augmented (80 ± 8 and 79 ± 10 mmHg; BCO+EMC and BCO+PMS, respectively; P < 0.05). However, summation of the individual MAP responses was greater than the response evoked during coactivation (106 ± 11 and 103 ± 12 mmHg, respectively, P < 0.05). Because summing the individual blood pressure responses exceeded the response during coactivation, the net effect was that the CSB and EPR interacted in an occlusive manner. In contrast, summation of the individual chronotropic responses was the same as the response evoked during coactivation. Moreover, there was no difference in summation of the individual MAP or HR responses when muscle afferents were activated by either EMC or PMS. In conclusion, the interaction between the CSB and the EPR in control of MAP was occlusive when both reflexes were stimulated to evoke sympathoexcitation. However, summation of the reflex changes in HR was simply additive.

AB - To determine the potential of an inhibitory interaction between the carotid sinus baroreflex (CSB) and the exercise pressor reflex (EPR), both pathways were activated to produce sympathoexcitation. It was hypothesized that, under conditions when the baroreflex increased sympathetic outflow, the interaction between CSB and EPR would be inhibitory. Bilateral carotid occlusion (BCO), electrically induced muscle contraction (EMC), and passive muscle stretch (PMS) were used to evoke sympathoexcitation. BCO decreased sinus pressure 50 ± 5 mmHg, and the levels of muscle tension generated by EMC and PMS were 7 ± 2 and 8 ± 1 kg, respectively. This resulted in significant increases in mean arterial pressure (MAP) of 55 ± 9, 50 ± 7, and 50 ± 6 mmHg (P = not significant, BCO vs. EMC vs. PMS) and in heart rate (HR) of 7 ± 2, 19 ± 4, and 17 ± 2 beats/min (P < 0.05, BCO vs. EMC and PMS). When BCO was combined with EMC or PMS, the reflex increase in MAP was augmented (80 ± 8 and 79 ± 10 mmHg; BCO+EMC and BCO+PMS, respectively; P < 0.05). However, summation of the individual MAP responses was greater than the response evoked during coactivation (106 ± 11 and 103 ± 12 mmHg, respectively, P < 0.05). Because summing the individual blood pressure responses exceeded the response during coactivation, the net effect was that the CSB and EPR interacted in an occlusive manner. In contrast, summation of the individual chronotropic responses was the same as the response evoked during coactivation. Moreover, there was no difference in summation of the individual MAP or HR responses when muscle afferents were activated by either EMC or PMS. In conclusion, the interaction between the CSB and the EPR in control of MAP was occlusive when both reflexes were stimulated to evoke sympathoexcitation. However, summation of the reflex changes in HR was simply additive.

KW - Baroreceptor afferents

KW - Blood pressure

KW - Exercise

KW - Heart rate

KW - Somatic afferents

KW - Static muscle contraction

KW - Sympathetic nerve activity

UR - http://www.scopus.com/inward/record.url?scp=0031919368&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031919368&partnerID=8YFLogxK

M3 - Article

C2 - 9516179

AN - SCOPUS:0031919368

VL - 84

SP - 1158

EP - 1165

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 0161-7567

IS - 4

ER -