Effects of graded oxygen tension on adenosine release by renal medullary and thick ascending limb suspensions

Robert E. Beach, Bruns Watts, David Good, Claude R. Benedict, Thomas D. DuBose

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Adenosine is released from renal cells, and extracellular adenosine may influence the effects of ischemia on medullary tubule segments by altering ion transport or renal hemodynamics. While adenosine release and excretion are enhanced during renal ischemia, the specific sites of renal adenosine production have not been completely elucidated. In the present study, extracellular adenosine concentrations in suspensions of renal outer medulla and thick ascending limb segments were quantitated by reversed-phase high performance liquid chromatography. Media from other medullary (OM) suspensions incubated for 8 and 15 minutes at 0% oxygen contained significantly greater amounts of adenosine (1.404 ± 0.21 and 2.034 ± 0.27 ng/μg protein, respectively), when compared to values obtained from media of suspensions incubated for equivalent periods under non-hypoxic conditions (8, 20, and 95% oxygen), 0.78 ± 0.05 (8 min) and 1.37 ± 0.21 ng/μg protein (15 min). Similarly, adenosine release was greater in medullary thick ascending limb (mTAL) suspensions incubated for 8 minutes at 0% versus 8% oxygen (0.81 ± 0.17 vs. 0.20 ± 0.12 ng/μg protein, respectively). Moreover, the observed increase in adenosine release by thick ascending limbs at 0% oxygen could be inhibited completely by either furosemide or ouabain. These studies demonstrate that: 1) the renal medulla and medullary thick ascending limb are sites of adenosine release; 2) adenosine release by the mTAL is enhanced significantly during hypoxic conditions; and 3) the increased release of adenosine during hypoxia appears to be related to ion transport and oxidative metabolism, as the increased release was prevented by two disparate inhibitors of transport in this segment.

Original languageEnglish (US)
Pages (from-to)836-842
Number of pages7
JournalKidney International
Volume39
Issue number5
StatePublished - May 1991
Externally publishedYes

Fingerprint

Adenosine
Suspensions
Extremities
Oxygen
Kidney
Ion Transport
Ischemia
Proteins
Furosemide
Ouabain
Reverse-Phase Chromatography
Hemodynamics
High Pressure Liquid Chromatography

ASJC Scopus subject areas

  • Nephrology

Cite this

Effects of graded oxygen tension on adenosine release by renal medullary and thick ascending limb suspensions. / Beach, Robert E.; Watts, Bruns; Good, David; Benedict, Claude R.; DuBose, Thomas D.

In: Kidney International, Vol. 39, No. 5, 05.1991, p. 836-842.

Research output: Contribution to journalArticle

@article{0e68656acbc44ec5a86ea5292dbb2338,
title = "Effects of graded oxygen tension on adenosine release by renal medullary and thick ascending limb suspensions",
abstract = "Adenosine is released from renal cells, and extracellular adenosine may influence the effects of ischemia on medullary tubule segments by altering ion transport or renal hemodynamics. While adenosine release and excretion are enhanced during renal ischemia, the specific sites of renal adenosine production have not been completely elucidated. In the present study, extracellular adenosine concentrations in suspensions of renal outer medulla and thick ascending limb segments were quantitated by reversed-phase high performance liquid chromatography. Media from other medullary (OM) suspensions incubated for 8 and 15 minutes at 0{\%} oxygen contained significantly greater amounts of adenosine (1.404 ± 0.21 and 2.034 ± 0.27 ng/μg protein, respectively), when compared to values obtained from media of suspensions incubated for equivalent periods under non-hypoxic conditions (8, 20, and 95{\%} oxygen), 0.78 ± 0.05 (8 min) and 1.37 ± 0.21 ng/μg protein (15 min). Similarly, adenosine release was greater in medullary thick ascending limb (mTAL) suspensions incubated for 8 minutes at 0{\%} versus 8{\%} oxygen (0.81 ± 0.17 vs. 0.20 ± 0.12 ng/μg protein, respectively). Moreover, the observed increase in adenosine release by thick ascending limbs at 0{\%} oxygen could be inhibited completely by either furosemide or ouabain. These studies demonstrate that: 1) the renal medulla and medullary thick ascending limb are sites of adenosine release; 2) adenosine release by the mTAL is enhanced significantly during hypoxic conditions; and 3) the increased release of adenosine during hypoxia appears to be related to ion transport and oxidative metabolism, as the increased release was prevented by two disparate inhibitors of transport in this segment.",
author = "Beach, {Robert E.} and Bruns Watts and David Good and Benedict, {Claude R.} and DuBose, {Thomas D.}",
year = "1991",
month = "5",
language = "English (US)",
volume = "39",
pages = "836--842",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "5",

}

TY - JOUR

T1 - Effects of graded oxygen tension on adenosine release by renal medullary and thick ascending limb suspensions

AU - Beach, Robert E.

AU - Watts, Bruns

AU - Good, David

AU - Benedict, Claude R.

AU - DuBose, Thomas D.

PY - 1991/5

Y1 - 1991/5

N2 - Adenosine is released from renal cells, and extracellular adenosine may influence the effects of ischemia on medullary tubule segments by altering ion transport or renal hemodynamics. While adenosine release and excretion are enhanced during renal ischemia, the specific sites of renal adenosine production have not been completely elucidated. In the present study, extracellular adenosine concentrations in suspensions of renal outer medulla and thick ascending limb segments were quantitated by reversed-phase high performance liquid chromatography. Media from other medullary (OM) suspensions incubated for 8 and 15 minutes at 0% oxygen contained significantly greater amounts of adenosine (1.404 ± 0.21 and 2.034 ± 0.27 ng/μg protein, respectively), when compared to values obtained from media of suspensions incubated for equivalent periods under non-hypoxic conditions (8, 20, and 95% oxygen), 0.78 ± 0.05 (8 min) and 1.37 ± 0.21 ng/μg protein (15 min). Similarly, adenosine release was greater in medullary thick ascending limb (mTAL) suspensions incubated for 8 minutes at 0% versus 8% oxygen (0.81 ± 0.17 vs. 0.20 ± 0.12 ng/μg protein, respectively). Moreover, the observed increase in adenosine release by thick ascending limbs at 0% oxygen could be inhibited completely by either furosemide or ouabain. These studies demonstrate that: 1) the renal medulla and medullary thick ascending limb are sites of adenosine release; 2) adenosine release by the mTAL is enhanced significantly during hypoxic conditions; and 3) the increased release of adenosine during hypoxia appears to be related to ion transport and oxidative metabolism, as the increased release was prevented by two disparate inhibitors of transport in this segment.

AB - Adenosine is released from renal cells, and extracellular adenosine may influence the effects of ischemia on medullary tubule segments by altering ion transport or renal hemodynamics. While adenosine release and excretion are enhanced during renal ischemia, the specific sites of renal adenosine production have not been completely elucidated. In the present study, extracellular adenosine concentrations in suspensions of renal outer medulla and thick ascending limb segments were quantitated by reversed-phase high performance liquid chromatography. Media from other medullary (OM) suspensions incubated for 8 and 15 minutes at 0% oxygen contained significantly greater amounts of adenosine (1.404 ± 0.21 and 2.034 ± 0.27 ng/μg protein, respectively), when compared to values obtained from media of suspensions incubated for equivalent periods under non-hypoxic conditions (8, 20, and 95% oxygen), 0.78 ± 0.05 (8 min) and 1.37 ± 0.21 ng/μg protein (15 min). Similarly, adenosine release was greater in medullary thick ascending limb (mTAL) suspensions incubated for 8 minutes at 0% versus 8% oxygen (0.81 ± 0.17 vs. 0.20 ± 0.12 ng/μg protein, respectively). Moreover, the observed increase in adenosine release by thick ascending limbs at 0% oxygen could be inhibited completely by either furosemide or ouabain. These studies demonstrate that: 1) the renal medulla and medullary thick ascending limb are sites of adenosine release; 2) adenosine release by the mTAL is enhanced significantly during hypoxic conditions; and 3) the increased release of adenosine during hypoxia appears to be related to ion transport and oxidative metabolism, as the increased release was prevented by two disparate inhibitors of transport in this segment.

UR - http://www.scopus.com/inward/record.url?scp=0025854979&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025854979&partnerID=8YFLogxK

M3 - Article

VL - 39

SP - 836

EP - 842

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - 5

ER -