Nitric oxide contributes to vascular smooth muscle relaxation in contracting fast-twitch muscles

Robert W. Grange, Eiji Isotani, Kim S. Lau, Kristine E. Kamm, Paul L. Huang, James T. Stull

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

During skeletal muscle contraction, NO derived from neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers or from endothelial cells (eNOS) may relax vascular smooth muscle contributing to functional hyperemia. To examine the relative importance of these pathways, smooth muscle myosin regulatory light chain (smRLC) phosphorylation was assessed as an index of vascular tone in isolated extensor digitorum longus (EDL) muscles from C57, nNOS-/-, and eNOS-/- mice. The smRLC phosphorylation (in mol phosphate per mol smRLC) in C57 resting muscles (0.12 ± 0.04) was increased 3.7-fold (0.44 ± 0.03) by phenylephrine (PE). Reversal of this increase with electrical stimulation (to 0.19 ± 0.03; P < 0.05) was partially blocked by Nω-nitro-L-arginine (NLA). In nNOS-/- EDL, the PE-induced increase in smRLC phosphorylation (0.10 ± 0.02 to 0.49 ± 0.04) was partially decreased by stimulation (0.25 ± 0.04). In eNOS-/- EDL, the control value for smRLC was increased (0.24 ± 0.04), and PE-induced smRLC phosphorylation (0.36 ± 0.06) was decreased by stimulation even in the presence of NLA (to 0.20 ± 0.02; P < 0.05). These results suggest that in addition to NO-independent mechanisms, NO derived from both nNOS and eNOS plays a role in the integrative vascular response of contracting skeletal muscle.

Original languageEnglish (US)
Pages (from-to)35-44
Number of pages10
JournalPhysiological Genomics
Volume2001
Issue number5
StatePublished - Jun 2001

Fingerprint

Smooth Muscle Myosins
Myosin Light Chains
Muscle Relaxation
Vascular Smooth Muscle
Nitric Oxide Synthase Type I
Nitric Oxide
Muscles
Phenylephrine
Endothelial Cells
Phosphorylation
Blood Vessels
Arginine
Skeletal Muscle
Skeletal Muscle Fibers
Hyperemia
Muscle Contraction
Electric Stimulation
Phosphates

Keywords

  • Endothelial nitric oxide synthase
  • Exercise hyperemia
  • Neuronal nitric oxide synthase
  • Skeletal muscle

ASJC Scopus subject areas

  • Genetics
  • Physiology

Cite this

Nitric oxide contributes to vascular smooth muscle relaxation in contracting fast-twitch muscles. / Grange, Robert W.; Isotani, Eiji; Lau, Kim S.; Kamm, Kristine E.; Huang, Paul L.; Stull, James T.

In: Physiological Genomics, Vol. 2001, No. 5, 06.2001, p. 35-44.

Research output: Contribution to journalArticle

Grange, Robert W. ; Isotani, Eiji ; Lau, Kim S. ; Kamm, Kristine E. ; Huang, Paul L. ; Stull, James T. / Nitric oxide contributes to vascular smooth muscle relaxation in contracting fast-twitch muscles. In: Physiological Genomics. 2001 ; Vol. 2001, No. 5. pp. 35-44.
@article{916ecefebee04b94ad24fc991075adc0,
title = "Nitric oxide contributes to vascular smooth muscle relaxation in contracting fast-twitch muscles",
abstract = "During skeletal muscle contraction, NO derived from neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers or from endothelial cells (eNOS) may relax vascular smooth muscle contributing to functional hyperemia. To examine the relative importance of these pathways, smooth muscle myosin regulatory light chain (smRLC) phosphorylation was assessed as an index of vascular tone in isolated extensor digitorum longus (EDL) muscles from C57, nNOS-/-, and eNOS-/- mice. The smRLC phosphorylation (in mol phosphate per mol smRLC) in C57 resting muscles (0.12 ± 0.04) was increased 3.7-fold (0.44 ± 0.03) by phenylephrine (PE). Reversal of this increase with electrical stimulation (to 0.19 ± 0.03; P < 0.05) was partially blocked by Nω-nitro-L-arginine (NLA). In nNOS-/- EDL, the PE-induced increase in smRLC phosphorylation (0.10 ± 0.02 to 0.49 ± 0.04) was partially decreased by stimulation (0.25 ± 0.04). In eNOS-/- EDL, the control value for smRLC was increased (0.24 ± 0.04), and PE-induced smRLC phosphorylation (0.36 ± 0.06) was decreased by stimulation even in the presence of NLA (to 0.20 ± 0.02; P < 0.05). These results suggest that in addition to NO-independent mechanisms, NO derived from both nNOS and eNOS plays a role in the integrative vascular response of contracting skeletal muscle.",
keywords = "Endothelial nitric oxide synthase, Exercise hyperemia, Neuronal nitric oxide synthase, Skeletal muscle",
author = "Grange, {Robert W.} and Eiji Isotani and Lau, {Kim S.} and Kamm, {Kristine E.} and Huang, {Paul L.} and Stull, {James T.}",
year = "2001",
month = "6",
language = "English (US)",
volume = "2001",
pages = "35--44",
journal = "Physiological Genomics",
issn = "1531-2267",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Nitric oxide contributes to vascular smooth muscle relaxation in contracting fast-twitch muscles

AU - Grange, Robert W.

AU - Isotani, Eiji

AU - Lau, Kim S.

AU - Kamm, Kristine E.

AU - Huang, Paul L.

AU - Stull, James T.

PY - 2001/6

Y1 - 2001/6

N2 - During skeletal muscle contraction, NO derived from neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers or from endothelial cells (eNOS) may relax vascular smooth muscle contributing to functional hyperemia. To examine the relative importance of these pathways, smooth muscle myosin regulatory light chain (smRLC) phosphorylation was assessed as an index of vascular tone in isolated extensor digitorum longus (EDL) muscles from C57, nNOS-/-, and eNOS-/- mice. The smRLC phosphorylation (in mol phosphate per mol smRLC) in C57 resting muscles (0.12 ± 0.04) was increased 3.7-fold (0.44 ± 0.03) by phenylephrine (PE). Reversal of this increase with electrical stimulation (to 0.19 ± 0.03; P < 0.05) was partially blocked by Nω-nitro-L-arginine (NLA). In nNOS-/- EDL, the PE-induced increase in smRLC phosphorylation (0.10 ± 0.02 to 0.49 ± 0.04) was partially decreased by stimulation (0.25 ± 0.04). In eNOS-/- EDL, the control value for smRLC was increased (0.24 ± 0.04), and PE-induced smRLC phosphorylation (0.36 ± 0.06) was decreased by stimulation even in the presence of NLA (to 0.20 ± 0.02; P < 0.05). These results suggest that in addition to NO-independent mechanisms, NO derived from both nNOS and eNOS plays a role in the integrative vascular response of contracting skeletal muscle.

AB - During skeletal muscle contraction, NO derived from neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers or from endothelial cells (eNOS) may relax vascular smooth muscle contributing to functional hyperemia. To examine the relative importance of these pathways, smooth muscle myosin regulatory light chain (smRLC) phosphorylation was assessed as an index of vascular tone in isolated extensor digitorum longus (EDL) muscles from C57, nNOS-/-, and eNOS-/- mice. The smRLC phosphorylation (in mol phosphate per mol smRLC) in C57 resting muscles (0.12 ± 0.04) was increased 3.7-fold (0.44 ± 0.03) by phenylephrine (PE). Reversal of this increase with electrical stimulation (to 0.19 ± 0.03; P < 0.05) was partially blocked by Nω-nitro-L-arginine (NLA). In nNOS-/- EDL, the PE-induced increase in smRLC phosphorylation (0.10 ± 0.02 to 0.49 ± 0.04) was partially decreased by stimulation (0.25 ± 0.04). In eNOS-/- EDL, the control value for smRLC was increased (0.24 ± 0.04), and PE-induced smRLC phosphorylation (0.36 ± 0.06) was decreased by stimulation even in the presence of NLA (to 0.20 ± 0.02; P < 0.05). These results suggest that in addition to NO-independent mechanisms, NO derived from both nNOS and eNOS plays a role in the integrative vascular response of contracting skeletal muscle.

KW - Endothelial nitric oxide synthase

KW - Exercise hyperemia

KW - Neuronal nitric oxide synthase

KW - Skeletal muscle

UR - http://www.scopus.com/inward/record.url?scp=0345876792&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0345876792&partnerID=8YFLogxK

M3 - Article

C2 - 11161004

AN - SCOPUS:0345876792

VL - 2001

SP - 35

EP - 44

JO - Physiological Genomics

JF - Physiological Genomics

SN - 1531-2267

IS - 5

ER -