Adenosine and free-flow functional hyperemia in striated muscle.

Kenneth G Proctor, B. R. Duling

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Striated muscle arteriolar responses to 1.5 min of 1-Hz contraction and/or increased tissue O2 partial pressure (PO2) were observed during exposure of the tissue interstitial space to adenosine deaminase (ADA) to evaluate the role of adenosine (ADO) as a regulator for blood flow. The microvasculature of the hamster cremaster muscle was continuously superfused with a bicarbonate buffer containing 11 micrograms ADA/ml and equilibrated with 5% CO2 and various O2 concentrations. Arterioles (resting diameter less than 30 micrometers) constricted a maximum of 55% when the superfusate gas tension was increased from 0 to 95% O2, but ADA had no effect on this behavior. Arterioles dilated during exercise, but the diameter change was decreased 20-25% during exercise with ADA treatment at both normal and elevated tissue PO2. As ADA had no effect on either the vasodilation to 2-chloroadenosine or resting arteriolar diameter, it was probably specific in its action. Assuming that all extracellular ADO was accessible to ADA and that ADA neutralized most newly formed ADO, we conclude that ADO is one component of a multifactor system mediating short periods of free-flow exercise hyperemia and that the release of ADO is not necessarily dependent on tissue hypoxia.

Original languageEnglish
JournalThe American journal of physiology
Volume242
Issue number4
StatePublished - Apr 1 1982
Externally publishedYes

Fingerprint

Adenosine Deaminase
Striated Muscle
Hyperemia
Adenosine
Arterioles
2-Chloroadenosine
Abdominal Muscles
Partial Pressure
Bicarbonates
Microvessels
Vasodilation
Cricetinae
Buffers
Gases

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Adenosine and free-flow functional hyperemia in striated muscle. / Proctor, Kenneth G; Duling, B. R.

In: The American journal of physiology, Vol. 242, No. 4, 01.04.1982.

Research output: Contribution to journalArticle

@article{837d32b06fab45cdaa7394c9a626acfc,
title = "Adenosine and free-flow functional hyperemia in striated muscle.",
abstract = "Striated muscle arteriolar responses to 1.5 min of 1-Hz contraction and/or increased tissue O2 partial pressure (PO2) were observed during exposure of the tissue interstitial space to adenosine deaminase (ADA) to evaluate the role of adenosine (ADO) as a regulator for blood flow. The microvasculature of the hamster cremaster muscle was continuously superfused with a bicarbonate buffer containing 11 micrograms ADA/ml and equilibrated with 5{\%} CO2 and various O2 concentrations. Arterioles (resting diameter less than 30 micrometers) constricted a maximum of 55{\%} when the superfusate gas tension was increased from 0 to 95{\%} O2, but ADA had no effect on this behavior. Arterioles dilated during exercise, but the diameter change was decreased 20-25{\%} during exercise with ADA treatment at both normal and elevated tissue PO2. As ADA had no effect on either the vasodilation to 2-chloroadenosine or resting arteriolar diameter, it was probably specific in its action. Assuming that all extracellular ADO was accessible to ADA and that ADA neutralized most newly formed ADO, we conclude that ADO is one component of a multifactor system mediating short periods of free-flow exercise hyperemia and that the release of ADO is not necessarily dependent on tissue hypoxia.",
author = "Proctor, {Kenneth G} and Duling, {B. R.}",
year = "1982",
month = "4",
day = "1",
language = "English",
volume = "242",
journal = "American Journal of Physiology - Cell Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "4",

}

TY - JOUR

T1 - Adenosine and free-flow functional hyperemia in striated muscle.

AU - Proctor, Kenneth G

AU - Duling, B. R.

PY - 1982/4/1

Y1 - 1982/4/1

N2 - Striated muscle arteriolar responses to 1.5 min of 1-Hz contraction and/or increased tissue O2 partial pressure (PO2) were observed during exposure of the tissue interstitial space to adenosine deaminase (ADA) to evaluate the role of adenosine (ADO) as a regulator for blood flow. The microvasculature of the hamster cremaster muscle was continuously superfused with a bicarbonate buffer containing 11 micrograms ADA/ml and equilibrated with 5% CO2 and various O2 concentrations. Arterioles (resting diameter less than 30 micrometers) constricted a maximum of 55% when the superfusate gas tension was increased from 0 to 95% O2, but ADA had no effect on this behavior. Arterioles dilated during exercise, but the diameter change was decreased 20-25% during exercise with ADA treatment at both normal and elevated tissue PO2. As ADA had no effect on either the vasodilation to 2-chloroadenosine or resting arteriolar diameter, it was probably specific in its action. Assuming that all extracellular ADO was accessible to ADA and that ADA neutralized most newly formed ADO, we conclude that ADO is one component of a multifactor system mediating short periods of free-flow exercise hyperemia and that the release of ADO is not necessarily dependent on tissue hypoxia.

AB - Striated muscle arteriolar responses to 1.5 min of 1-Hz contraction and/or increased tissue O2 partial pressure (PO2) were observed during exposure of the tissue interstitial space to adenosine deaminase (ADA) to evaluate the role of adenosine (ADO) as a regulator for blood flow. The microvasculature of the hamster cremaster muscle was continuously superfused with a bicarbonate buffer containing 11 micrograms ADA/ml and equilibrated with 5% CO2 and various O2 concentrations. Arterioles (resting diameter less than 30 micrometers) constricted a maximum of 55% when the superfusate gas tension was increased from 0 to 95% O2, but ADA had no effect on this behavior. Arterioles dilated during exercise, but the diameter change was decreased 20-25% during exercise with ADA treatment at both normal and elevated tissue PO2. As ADA had no effect on either the vasodilation to 2-chloroadenosine or resting arteriolar diameter, it was probably specific in its action. Assuming that all extracellular ADO was accessible to ADA and that ADA neutralized most newly formed ADO, we conclude that ADO is one component of a multifactor system mediating short periods of free-flow exercise hyperemia and that the release of ADO is not necessarily dependent on tissue hypoxia.

UR - http://www.scopus.com/inward/record.url?scp=0020120874&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020120874&partnerID=8YFLogxK

M3 - Article

C2 - 7065281

AN - SCOPUS:0020120874

VL - 242

JO - American Journal of Physiology - Cell Physiology

JF - American Journal of Physiology - Cell Physiology

SN - 0363-6143

IS - 4

ER -