Hindlimb venous distention evokes a pressor reflex in decerebrated rats

Katsuya Yamauchi, Audrey J. Stone, Marc P Kaufman

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The distention of small vessels caused by an increase in blood flow to dynamically exercising muscles has been proposed as a stimulus that activates the thin fiber (groups III and IV) afferents evoking the exercise pressor reflex. This theory has been supported by evidence obtained from both humans and animals. In decerebrated unanesthetized rats with either freely perfused femoral arteries or arteries that were ligated 3 days before the experiment, we attempted to provide evidence in support of this theory by measuring arterial pressure, heart rate, and renal sympathetic nerve discharge while retrogradely injecting Ringer’s solution in increasing volumes into the femoral vein just as it excited the triceps surae muscles. We found that the pressor response to injection was directly proportional to the volume injected. Retrograde injection of volumes up to and including 1 mL had no significant effect on either heart rate or renal sympathetic nerve activity. Cyclooxygenase blockade with indomethacin attenuated the reflex pressor response to retrograde injection in both groups of rats. In contrast, gadolinium, which blocks mechanogated channels, attenuated the reflex pressor response to retrograde injection in the “ligated rats,” but had no effect on the response in “freely perfused” rats. Our findings are consistent with the possibility that distension of small vessels within exercising skeletal muscle can serve as a stimulus to the thin fiber afferents evoking the exercise pressor reflex.

Original languageEnglish (US)
Article numbere12036
JournalPhysiological Reports
Volume2
Issue number6
DOIs
StatePublished - 2014
Externally publishedYes

Fingerprint

Hindlimb
Reflex
Injections
Heart Rate
Kidney
Muscles
Femoral Vein
Gadolinium
Femoral Artery
Prostaglandin-Endoperoxide Synthases
Indomethacin
Arterial Pressure
Skeletal Muscle
Arteries

Keywords

  • Autonomic nervous system
  • Dynamic exercise
  • Peripheral artery disease
  • Thin fiber muscle afferents

ASJC Scopus subject areas

  • Physiology (medical)
  • Physiology

Cite this

Hindlimb venous distention evokes a pressor reflex in decerebrated rats. / Yamauchi, Katsuya; Stone, Audrey J.; Kaufman, Marc P.

In: Physiological Reports, Vol. 2, No. 6, e12036, 2014.

Research output: Contribution to journalArticle

@article{9cda38b819c8479ebf375a538c2eec87,
title = "Hindlimb venous distention evokes a pressor reflex in decerebrated rats",
abstract = "The distention of small vessels caused by an increase in blood flow to dynamically exercising muscles has been proposed as a stimulus that activates the thin fiber (groups III and IV) afferents evoking the exercise pressor reflex. This theory has been supported by evidence obtained from both humans and animals. In decerebrated unanesthetized rats with either freely perfused femoral arteries or arteries that were ligated 3 days before the experiment, we attempted to provide evidence in support of this theory by measuring arterial pressure, heart rate, and renal sympathetic nerve discharge while retrogradely injecting Ringer’s solution in increasing volumes into the femoral vein just as it excited the triceps surae muscles. We found that the pressor response to injection was directly proportional to the volume injected. Retrograde injection of volumes up to and including 1 mL had no significant effect on either heart rate or renal sympathetic nerve activity. Cyclooxygenase blockade with indomethacin attenuated the reflex pressor response to retrograde injection in both groups of rats. In contrast, gadolinium, which blocks mechanogated channels, attenuated the reflex pressor response to retrograde injection in the “ligated rats,” but had no effect on the response in “freely perfused” rats. Our findings are consistent with the possibility that distension of small vessels within exercising skeletal muscle can serve as a stimulus to the thin fiber afferents evoking the exercise pressor reflex.",
keywords = "Autonomic nervous system, Dynamic exercise, Peripheral artery disease, Thin fiber muscle afferents",
author = "Katsuya Yamauchi and Stone, {Audrey J.} and Kaufman, {Marc P}",
year = "2014",
doi = "10.14814/phy2.12036",
language = "English (US)",
volume = "2",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "John Wiley and Sons Inc.",
number = "6",

}

TY - JOUR

T1 - Hindlimb venous distention evokes a pressor reflex in decerebrated rats

AU - Yamauchi, Katsuya

AU - Stone, Audrey J.

AU - Kaufman, Marc P

PY - 2014

Y1 - 2014

N2 - The distention of small vessels caused by an increase in blood flow to dynamically exercising muscles has been proposed as a stimulus that activates the thin fiber (groups III and IV) afferents evoking the exercise pressor reflex. This theory has been supported by evidence obtained from both humans and animals. In decerebrated unanesthetized rats with either freely perfused femoral arteries or arteries that were ligated 3 days before the experiment, we attempted to provide evidence in support of this theory by measuring arterial pressure, heart rate, and renal sympathetic nerve discharge while retrogradely injecting Ringer’s solution in increasing volumes into the femoral vein just as it excited the triceps surae muscles. We found that the pressor response to injection was directly proportional to the volume injected. Retrograde injection of volumes up to and including 1 mL had no significant effect on either heart rate or renal sympathetic nerve activity. Cyclooxygenase blockade with indomethacin attenuated the reflex pressor response to retrograde injection in both groups of rats. In contrast, gadolinium, which blocks mechanogated channels, attenuated the reflex pressor response to retrograde injection in the “ligated rats,” but had no effect on the response in “freely perfused” rats. Our findings are consistent with the possibility that distension of small vessels within exercising skeletal muscle can serve as a stimulus to the thin fiber afferents evoking the exercise pressor reflex.

AB - The distention of small vessels caused by an increase in blood flow to dynamically exercising muscles has been proposed as a stimulus that activates the thin fiber (groups III and IV) afferents evoking the exercise pressor reflex. This theory has been supported by evidence obtained from both humans and animals. In decerebrated unanesthetized rats with either freely perfused femoral arteries or arteries that were ligated 3 days before the experiment, we attempted to provide evidence in support of this theory by measuring arterial pressure, heart rate, and renal sympathetic nerve discharge while retrogradely injecting Ringer’s solution in increasing volumes into the femoral vein just as it excited the triceps surae muscles. We found that the pressor response to injection was directly proportional to the volume injected. Retrograde injection of volumes up to and including 1 mL had no significant effect on either heart rate or renal sympathetic nerve activity. Cyclooxygenase blockade with indomethacin attenuated the reflex pressor response to retrograde injection in both groups of rats. In contrast, gadolinium, which blocks mechanogated channels, attenuated the reflex pressor response to retrograde injection in the “ligated rats,” but had no effect on the response in “freely perfused” rats. Our findings are consistent with the possibility that distension of small vessels within exercising skeletal muscle can serve as a stimulus to the thin fiber afferents evoking the exercise pressor reflex.

KW - Autonomic nervous system

KW - Dynamic exercise

KW - Peripheral artery disease

KW - Thin fiber muscle afferents

UR - http://www.scopus.com/inward/record.url?scp=85003491703&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85003491703&partnerID=8YFLogxK

U2 - 10.14814/phy2.12036

DO - 10.14814/phy2.12036

M3 - Article

AN - SCOPUS:85003491703

VL - 2

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 6

M1 - e12036

ER -