Role of nitric oxide in exercise-induced vasodilation in man

Koller-Strametz, J; Matulla, Bettina; Wolzt, Michael; Müller, Markus; Entlicher, Jesusa; Eichler, Hans‐Georg; Schmetterer, Leopold

doi:10.1016/s0024-3205(98)00024-1

Cited by 25 publications

(19 citation statements)

References 34 publications

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“…It consists of interacting entities including: cones and rods as sensors, bipolar and horizontal cells as primary modulators, retinal ganglion cells as connectors, neuromediators as information transfer, local and systemic vascular mediators as actuators In contrast to other studies investigating the neurovascular coupling effects [8,9,25,26,17,28,39,40,41,42], we attempted to characterize the time course of the vessel reaction in response to the stimulus. Since this is a biological control process, it consists of different phases known from technical control processes (Figs.…”

Section: Discussionmentioning

confidence: 99%

“…Hence, the vessel diameter response was primarily an answer to the change in luminance. According to the experimental design, lu- 17 Green monochromatic flicker (12 Hz, 10 s)-induced retinal arterial diameter response. Equal flicker stimuli were applied successively with constant pauses to assess baseline behavior.…”

Section: Retinal Vessel Reaction Depending On Flicker Colormentioning

confidence: 99%

“…Recent investigations with techniques assessing ocular blood flow have shown that such a mechanism operates at the optic nerve head and retina in cats [5,18,38,36,47,51], rabbits [50], mini-pigs [31], primates [2,3,15] and humans [8,9,10,11,12,13,14,17,25,26,27,28,30,32,31,33,39,40,41,42,44,45,52].…”

Section: Introductionmentioning

confidence: 99%

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Retinal vessel reaction in response to chromatic flickering light

Kotliar

Vilser

Nagel

et al. 2004

Graefe's Arch Clin Exp Ophthalmol

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Section: Discussionmentioning

confidence: 99%

Section: Retinal Vessel Reaction Depending On Flicker Colormentioning

confidence: 99%

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Retinal vessel reaction in response to chromatic flickering light

Kotliar

Vilser

Nagel

et al. 2004

Graefe's Arch Clin Exp Ophthalmol

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show abstract

“…A number of studies, in which NOS has been inhibited with L-NMMA, have demonstrated that NO is important for blood flow to human skeletal muscle at rest [1, 2, 3, 4]and in the recovery phase after muscle contractions [4, 29], whereas the blood flow rate during exercise is unaffected by L-NMMA administration [1, 2, 3, 4, 30]. The present findings of similar blood flows during exercise in controls and L-NAME are in accordance with these observations and, consequently, with the proposition that NO does not play an important role in the regulation of muscle blood flow during exercise.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have reported that inhibition of nitric oxide synthase (NOS) in humans by systemic administration of the L -arginine analog N G -monomethyl- L -arginine (L-NMMA) [1, 2, 3, 4, 5]does not affect the rate of blood flow in contracting skeletal muscle. This finding may simply reflect a lack of importance of nitric oxide (NO) in the regulation of muscle blood flow during exercise.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Nitric Oxide Synthesis by Systemic N<sup>G</sup>-Monomethyl-<i>L</i>-Arginine Administration in Humans: Effects on Interstitial Adenosine, Prostacyclin and Potassium Concentrations in Resting and Contracting Skeletal Muscle

Bangsbo¹,

Langberg²,

Saltin³

et al. 2000

J Vasc Res

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We examined whether the formation or the release of the vasodilators adenosine, prostacyclin (PGI₂) and potassium (K⁺) increase in skeletal muscle interstitium in response to nitric oxide synthase (NOS) inhibition. Five subjects performed one-legged knee extensor exercise at 30 W without (controls) and with prior N^G-nitro-L-arginine methyl ester (L-NAME) infusion (4 mg/kg, intravenously). Samples from the interstitial fluid were obtained at rest, during exercise and after exercise with the microdialysis technique. Interstitial adenosine in controls increased (p < 0.05) from 0.11 ± 0.03 μmol/l at rest to 0.48 ± 0.06 μmol/l during exercise. Interstitial adenosine during exercise in L-NAME was similar (p > 0.05) to controls. The 6-keto-prostaglandin F1α concentration in controls was 1.17 ± 0.20 ng/ml at rest and increased (p < 0.05) to 1.97 ± 0.30 ng/ml during exercise and was further elevated (p < 0.05) to 2.76 ± 0.38 ng/ml after exercise and these concentrations were not different (p > 0.05) in L-NAME. The interstitial K⁺ concentration in controls increased (p < 0.05) from 4.1 ± 0.1 mmol/l at rest to 9.5 ± 0.5 mmol/l during exercise. The interstitial K⁺ concentration during exercise (6.7 ± 0.4 mmol/l) was lower (p < 0.05) in L-NAME than in controls. The present findings demonstrate that the muscle interstitial concentrations of adenosine, PGI₂ and K⁺ during exercise are not increased with systemic NOS inhibition. Thus, the lack of effect of NOS inhibition on the rate of blood flow to contracting human skeletal muscle does not appear to be due to compensatory formation or release of adenosine, PGI₂ and K⁺ in the muscle interstitium. The present study also supports a role for PGI₂ in the regulation of blood flow during exercise.