No role of interstitial adenosine in insulin-mediated vasodilation

F Dela; B Stallknecht

No role of interstitial adenosine in insulin-mediated vasodilation

F Dela, B Stallknecht

Torekov Group

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

3 Citationer (Scopus)

Abstract

Udgivelsesdato: 1999-Sep

Originalsprog	Engelsk
Tidsskrift	Acta physiologica Scandinavica
Vol/bind	167
Udgave nummer	1
Sider (fra-til)	37-42
Antal sider	5
ISSN	0001-6772
Status	Udgivet - 1999

Bibliografisk note

Keywords: Adenosine; Adult; Humans; Hypoglycemic Agents; Insulin; Male; Muscle, Skeletal; Spinal Cord Injuries; Vasodilation

Citationsformater

@article{e57c4a30779311df928f000ea68e967b,

title = "No role of interstitial adenosine in insulin-mediated vasodilation",

abstract = "The mechanisms behind the vasodilatory effect of insulin are not fully understood, but nitric oxide plays an important role. We have investigated the possibility that insulin mediates vasodilatation in the human skeletal muscle via an increase in extracellular adenosine concentrations. In eight healthy subjects (H) and in four subjects with a complete, high (C5-C6/7) spinal cord injury (SCI) a hyperinsulinaemic (480 mU min-1 kg-1), isoglycaemic clamp was performed. SCI subjects were included as it has been proposed that adenosine and adenine nucleotides may be released from nerve endings in the skeletal muscle. Adenosine concentrations in the extracellular fluid (ECF) of skeletal muscle in the thigh were measured by means of the microdialysis technique. Leg blood flow (LBF) was measured by termodilution. In response to insulin infusion, LBF always increased (P < 0.05) (from 228 +/- 25 and 318 +/- 18 mL min-1 to 451 +/- 41 and 530 +/- 29 mL min-1, SCI and H, respectively [mean +/- SEM]). Concentrations of adenosine in the muscle ECF did not change with infusion of insulin and did not differ between groups (before: 147 +/- 55 [SCI] and 207 +/- 108 [H] nmol L-1; during: 160 +/- 36 [SCI] and 165 +/- 74 [H] nmol L-1). No significant correlation between concentrations of adenosine and corresponding LBF rates was achieved (LBF=[-0.0936. Adenosine] + 475. R=-0.092, P=0.22, number of samples=181, number of subjects=12). Conclusion: the mechanism by which insulin mediates an increase in skeletal muscle blood flow is not associated with adenosine in the ECF.",

author = "F Dela and B Stallknecht",

note = "Keywords: Adenosine; Adult; Humans; Hypoglycemic Agents; Insulin; Male; Muscle, Skeletal; Spinal Cord Injuries; Vasodilation",

year = "1999",

language = "English",

volume = "167",

pages = "37--42",

journal = "Acta physiologica Scandinavica",

issn = "0001-6772",

publisher = "Blackwell Science Ltd.",

number = "1",

}

TY - JOUR

T1 - No role of interstitial adenosine in insulin-mediated vasodilation

AU - Dela, F

AU - Stallknecht, B

N1 - Keywords: Adenosine; Adult; Humans; Hypoglycemic Agents; Insulin; Male; Muscle, Skeletal; Spinal Cord Injuries; Vasodilation

PY - 1999

Y1 - 1999

N2 - The mechanisms behind the vasodilatory effect of insulin are not fully understood, but nitric oxide plays an important role. We have investigated the possibility that insulin mediates vasodilatation in the human skeletal muscle via an increase in extracellular adenosine concentrations. In eight healthy subjects (H) and in four subjects with a complete, high (C5-C6/7) spinal cord injury (SCI) a hyperinsulinaemic (480 mU min-1 kg-1), isoglycaemic clamp was performed. SCI subjects were included as it has been proposed that adenosine and adenine nucleotides may be released from nerve endings in the skeletal muscle. Adenosine concentrations in the extracellular fluid (ECF) of skeletal muscle in the thigh were measured by means of the microdialysis technique. Leg blood flow (LBF) was measured by termodilution. In response to insulin infusion, LBF always increased (P < 0.05) (from 228 +/- 25 and 318 +/- 18 mL min-1 to 451 +/- 41 and 530 +/- 29 mL min-1, SCI and H, respectively [mean +/- SEM]). Concentrations of adenosine in the muscle ECF did not change with infusion of insulin and did not differ between groups (before: 147 +/- 55 [SCI] and 207 +/- 108 [H] nmol L-1; during: 160 +/- 36 [SCI] and 165 +/- 74 [H] nmol L-1). No significant correlation between concentrations of adenosine and corresponding LBF rates was achieved (LBF=[-0.0936. Adenosine] + 475. R=-0.092, P=0.22, number of samples=181, number of subjects=12). Conclusion: the mechanism by which insulin mediates an increase in skeletal muscle blood flow is not associated with adenosine in the ECF.

AB - The mechanisms behind the vasodilatory effect of insulin are not fully understood, but nitric oxide plays an important role. We have investigated the possibility that insulin mediates vasodilatation in the human skeletal muscle via an increase in extracellular adenosine concentrations. In eight healthy subjects (H) and in four subjects with a complete, high (C5-C6/7) spinal cord injury (SCI) a hyperinsulinaemic (480 mU min-1 kg-1), isoglycaemic clamp was performed. SCI subjects were included as it has been proposed that adenosine and adenine nucleotides may be released from nerve endings in the skeletal muscle. Adenosine concentrations in the extracellular fluid (ECF) of skeletal muscle in the thigh were measured by means of the microdialysis technique. Leg blood flow (LBF) was measured by termodilution. In response to insulin infusion, LBF always increased (P < 0.05) (from 228 +/- 25 and 318 +/- 18 mL min-1 to 451 +/- 41 and 530 +/- 29 mL min-1, SCI and H, respectively [mean +/- SEM]). Concentrations of adenosine in the muscle ECF did not change with infusion of insulin and did not differ between groups (before: 147 +/- 55 [SCI] and 207 +/- 108 [H] nmol L-1; during: 160 +/- 36 [SCI] and 165 +/- 74 [H] nmol L-1). No significant correlation between concentrations of adenosine and corresponding LBF rates was achieved (LBF=[-0.0936. Adenosine] + 475. R=-0.092, P=0.22, number of samples=181, number of subjects=12). Conclusion: the mechanism by which insulin mediates an increase in skeletal muscle blood flow is not associated with adenosine in the ECF.

M3 - Journal article

C2 - 10519975

SN - 0001-6772

VL - 167

SP - 37

EP - 42

JO - Acta physiologica Scandinavica

JF - Acta physiologica Scandinavica

IS - 1

ER -