Multiple dilator pathways in skeletal muscle contraction-induced arteriolar dilations

2002 ◽  
Vol 282 (4) ◽  
pp. R969-R978 ◽  
Author(s):  
Coral L. Murrant ◽  
Ingrid H. Sarelius
Keyword(s):  
Muscle Contraction ◽  
Muscle Fibers ◽  
No Synthase ◽  
Remote Site ◽  
Receptor Stimulation ◽  
Upstream Site ◽  
Local Site ◽  
Maximal Diameter ◽  
Skeletal Muscle Contraction ◽  
Synthase Inhibitor

To determine whether nitric oxide (NO), adenosine (Ado) receptors, or ATP-sensitive potassium (KATP) channels play a role in arteriolar dilations induced by muscle contraction, we used a cremaster preparation in anesthetesized hamsters in which we stimulated four to five muscle fibers lying perpendicular to a transverse arteriole (maximal diameter ∼35–65 μm). The diameter of the arteriole at the site of overlap of the stimulated muscle fibers (the local site) and at a remote site ∼1,000 μm upstream (the upstream site) was measured before, during, and after muscle contraction. Two minutes of 4-Hz muscle stimulation (5–15 V, 0.4 ms) produced local and upstream dilations of 19 ± 1 and 10 ± 1 μm, respectively. N ω-nitro-l-arginine (10−4 M; NO synthase inhibitor), xanthine amine congener (XAC; 10−6 M; Ado A1, A2A, and A2B receptor antagonist), or glibenclamide (Glib; 10−5 M; KATP channel inhibitor) superfused over the preparation attenuated the local dilation (by 29.7 ± 12.7, 61.8 ± 9.0, and 51.9 ± 14.9%, respectively), but only XAC and Glib attenuated the upstream dilation (by 68.9 ± 6.8 and 89.1 ± 6.4%, respectively). Furthermore, only Glib, when applied to the upstream site directly, attenuated the upstream dilation (48.1 ± 9.1%). Neither XAC nor Glib applied directly to the arteriole between the local and the upstream sites had an effect on the magnitude of the upstream dilation. We conclude that NO, Ado receptors, and KATP channels are involved in the local dilation initiated by contracting muscle and that both KATP channels and Ado receptor stimulation, but not NO, play a role in the manifestation of the dilation at the upstream site.

Local and remote arteriolar dilations initiated by skeletal muscle contraction

2000 ◽  
Vol 279 (5) ◽  
pp. H2285-H2294 ◽  
Author(s):  
Coral L. Murrant ◽  
Ingrid H. Sarelius
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Muscle Metabolism ◽  
Cremaster Muscle ◽  
Remote Site ◽  
Upstream Site ◽  
Skeletal Muscle Contraction ◽  
Perivascular Nerves ◽  
The Relationship

To investigate the relationship between skeletal muscle metabolism and arteriolar dilations in the region local to contracting muscle fibers as well as dilations at remote arteriolar regions upstream, we used a microelectrode on cremaster muscle of anesthetized hamsters to stimulate four to five muscle fibers lying approximately perpendicular to and overlapping a transverse arteriole. Before, during, and after muscle contraction, we measured the diameter of the arteriole at the site of muscle fiber overlap (local) and at a remote site ∼1,000 μm upstream. Two minutes of 2-, 4-, or 8-Hz stimulation (5–10 V, 0.4-ms duration) produced a significant dilation locally (8.2 ± 2.0-, 22.5 ± 2.4-, and 30.9 ± 2.1-μm increase, respectively) and at the remote site (4.2 ± 0.8, 11.0 ± 1.1, and 18.9 ± 2.7 μm, respectively). Muscle contraction at 4 Hz initiated a remote dilation that was unaffected by 15-min micropipette application of either 2 μM tetrodotoxin, 0.07% halothane, or 40 μM 18-β-glycyrrhetinic acid between the local and upstream site. Therefore, at the arteriolar level, muscle contraction initiates a robust remote dilation that does not appear to be transmitted via perivascular nerves or gap junctions.

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

2009 ◽  
Vol 297 (1) ◽  
pp. H433-H442 ◽  
Author(s):  
Ashok K. Dua ◽  
Nickesh Dua ◽  
Coral L. Murrant
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Nitric Oxide Donor ◽  
Contraction Frequency ◽  
Skeletal Muscle Contraction ◽  
Train Duration ◽  
Arteriolar Vasodilation ◽  
40 Hz

To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated four to five skeletal muscle fibers in the anesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibers. Diameter was measured before, during, and after 2 min of skeletal muscle contraction stimulated over a range of stimulus frequencies [4, 20, and 40 Hz; 15 contractions/min (cpm), 250 ms train duration] and a range of contraction frequencies (6, 15, and 60 cpm; 20 Hz stimulus frequency, 250 ms train duration). Muscle fibers were stimulated in the absence and presence of an inhibitor of adenosine receptors [10−6 M xanthine amine congener (XAC)], an ATP-dependent potassium (K+) channel inhibitor (10−5 M glibenclamide), an inhibitor of a source of K+ by inhibition of voltage-dependent K+ channels [3 × 10−4 M 3,4-diaminopyridine (DAP)], and an inhibitor of nitric oxide synthase [10−6 M NG-nitro-l-arginine methyl ester (l-NAME) + 10−7 S-nitroso- N-acetylpenicillamine (a nitric oxide donor)]. l-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60 cpm. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40 Hz. Glibenclamide inhibited all dilations at all stimulus and contraction frequencies, and DAP did not inhibit dilations at any stimulus frequencies while attenuating dilation at a contraction frequency of 60 cpm only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency; therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia.

Diaphragmatic lymphatic vessel behavior during local skeletal muscle contraction

2015 ◽  
Vol 308 (3) ◽  
pp. H193-H205 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Lymphatic Vessel ◽  
Muscle Fibers ◽  
Video Recording ◽  
Three Dimensional ◽  
Longitudinal Axis ◽  
Vessel Diameter ◽  
Skeletal Muscle Contraction ◽  
Lymphatic Network

The mechanism through which the stresses developed in the diaphragmatic tissue during skeletal muscle contraction sustain local lymphatic function was studied in 10 deeply anesthetized, tracheotomized adult Wistar rats whose diaphragm was exposed after thoracotomy. To evaluate the direct effect of skeletal muscle contraction on the hydraulic intraluminal lymphatic pressures (Plymph) and lymphatic vessel geometry, the maximal contraction of diaphragmatic fibers adjacent to a lymphatic vessel was elicited by injection of 9.2 nl of 1 M KCl solution among diaphragmatic fibers while Plymph was recorded through micropuncture and vessel geometry via stereomicroscopy video recording. In lymphatics oriented perpendicularly to the longitudinal axis of muscle fibers and located at <300 μm from KCl injection, vessel diameter at maximal skeletal muscle contraction ( Dmc) decreased to 61.3 ± 1.4% of the precontraction value [resting diameter ( Drest)]; however, if injection was at >900 μm from the vessel, Dmc enlarged to 131.1 ± 2.3% of Drest. In vessels parallel to muscle fibers, Dmc increased to 122.8 ± 2.9% of Drest. During contraction, Plymph decreased as much as 22.5 ± 2.6 cmH2O in all submesothelial superficial vessels, whereas it increased by 10.7 ± 5.1 cmH2O in deeper vessels running perpendicular to contracting muscle fibers. Hence, the three-dimensional arrangement of the diaphragmatic lymphatic network seems to be finalized to efficiently exploit the stresses exerted by muscle fibers during the contracting inspiratory phase to promote lymph formation in superficial submesothelial lymphatics and its further propulsion in deeper intramuscular vessels.

scholarly journals Lymph flow pattern in pleural diaphragmatic lymphatics during intrinsic and extrinsic isotonic contraction

2016 ◽  
Vol 310 (1) ◽  
pp. H60-H70 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Skeletal Muscle ◽  
Shear Stress ◽  
Muscle Contraction ◽  
Ex Vivo ◽  
Muscle Fibers ◽  
Lymphatic Vessels ◽  
Smooth Muscle Contraction ◽  
Skeletal Muscle Fibers ◽  
Skeletal Muscle Contraction

Peripheral rat diaphragmatic lymphatic vessels, endowed with intrinsic spontaneous contractility, were in vivo filled with fluorescent dextrans and microspheres and subsequently studied ex vivo in excised diaphragmatic samples. Changes in diameter and lymph velocity were detected, in a vessel segment, during spontaneous lymphatic smooth muscle contraction and upon activation, through electrical whole-field stimulation, of diaphragmatic skeletal muscle fibers. During intrinsic contraction lymph flowed both forward and backward, with a net forward propulsion of 14.1 ± 2.9 μm at an average net forward speed of 18.0 ± 3.6 μm/s. Each skeletal muscle contraction sustained a net forward-lymph displacement of 441.9 ± 159.2 μm at an average velocity of 339.9 ± 122.7 μm/s, values significantly higher than those documented during spontaneous contraction. The flow velocity profile was parabolic during both spontaneous and skeletal muscle contraction, and the shear stress calculated at the vessel wall at the highest instantaneous velocity never exceeded 0.25 dyne/cm2. Therefore, we propose that the synchronous contraction of diaphragmatic skeletal muscle fibers recruited at every inspiratory act dramatically enhances diaphragmatic lymph propulsion, whereas the spontaneous lymphatic contractility might, at least in the diaphragm, be essential in organizing the pattern of flow redistribution within the diaphragmatic lymphatic circuit. Moreover, the very low shear stress values observed in diaphragmatic lymphatics suggest that, in contrast with other contractile lymphatic networks, a likely interplay between intrinsic and extrinsic mechanisms be based on a mechanical and/or electrical connection rather than on nitric oxide release.

EDHF, but not NO or prostaglandins, is critical to evoke a conducted dilation upon ACh in hamster arterioles

2002 ◽  
Vol 283 (3) ◽  
pp. H996-H1004 ◽  
Author(s):  
Bernd Hoepfl ◽  
Barbara Rodenwaldt ◽  
Ulrich Pohl ◽  
Cor de Wit
Keyword(s):  
Vascular Wall ◽  
Additional Treatment ◽  
No Synthase ◽  
No Donor ◽  
Upstream Site ◽  
Local Site ◽  
Vascular Segment ◽  
Remote Sites ◽  
Cytochrome P 450 ◽  
Local Stimulation

Vasomotor reactions upon focal stimulation of arterioles have been shown to be conducted along the vascular wall. Such a conduction, which is assumed to reflect the spread of electrical signals, may contribute to coordination of responses within a vascular segment. We aimed to identify which endothelial autacoid(s) act as mediators of the local and conducted dilator responses, respectively. To this end, arterioles in the hamster cremaster microcirculation were locally stimulated with endothelium-dependent [acetylcholine (ACh)] or endothelium-independent dilators [sodium nitroprusside (SNP)], and the resulting changes in diameter were measured using a videomicroscopy technique at the site of application and up to 1.4 mm upstream at distant sites. Experiments were also performed after blockade of nitric oxide (NO) synthase, cyclooxygenase, P-450 monooxygenase, or K+ channels. Dilations upon ACh (71 ± 3%) were conducted rapidly (<1 s) to upstream sites (at 1.4 mm: 37 ± 5%). Although the NO donor SNP induced a similar local dilation (71 ± 7%), this response was not conducted. Maximal amplitudes of ACh-induced dilations were not attenuated after inhibition of NO synthase and cyclooxygenase at the local and remote sites. However, additional treatment with a P-450 monooxygenase blocker (sulfaphenazole) strongly attenuated the local response (from 62 ± 9 to 17 ± 5%) and abrogated dilations at distant sites (at 0.67 mm: from 23 ± 4% to 4 ± 3%). Likewise, 17-octadecynoic acid strongly attenuated local and remote responses. Blockers of Ca2+-dependent K+ channels (charybdotoxin or iberiotoxin) attenuated dilations at the local and remote sites after focal application at the ACh stimulation site. In marked contrast, treatment of the upstream site with these blockers was without any effect. We conclude that upon local stimulation with ACh, a cytochrome P-450 monooxygenase product is generated that induces local dilation via the activation of Ca2+-dependent K+ channels and initiates conduction of the dilation. In contrast to the local site, neither activation of these K+channels nor the synthesis of NO or prostaglandins is necessary to dilate the arterioles at remote, distant sites. This suggests that endothelium-derived hyperpolarizing factor serves as an important mediator to initiate conducted dilations and, by doing so, may act as a key player in the coordination of arteriolar behavior in the microcirculatory network.

Phosphorylation of the regulatory light chains of myosin affects Ca2+sensitivity of skeletal muscle contraction

2002 ◽  
Vol 92 (4) ◽  
pp. 1661-1670 ◽  
Author(s):  
Danuta Szczesna ◽  
Jiaju Zhao ◽  
Michelle Jones ◽  
Gang Zhi ◽  
James Stull ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Light Chains ◽  
Regulatory Light Chains ◽  
Force Development ◽  
Skeletal Muscle Contraction ◽  
State Force ◽  
Kinetics Of

The role of phosphorylation of the myosin regulatory light chains (RLC) is well established in smooth muscle contraction, but in striated (skeletal and cardiac) muscle its role is still controversial. We have studied the effects of RLC phosphorylation in reconstituted myosin and in skinned skeletal muscle fibers where Ca2+sensitivity and the kinetics of steady-state force development were measured. Skeletal muscle myosin reconstituted with phosphorylated RLC produced a much higher Ca2+sensitivity of thin filament-regulated ATPase activity than nonphosphorylated RLC (change in −log of the Ca2+concentration producing half-maximal activation = ∼0.25). The same was true for the Ca2+sensitivity of force in skinned skeletal muscle fibers, which increased on reconstitution of the fibers with the phosphorylated RLC. In addition, we have shown that the level of endogenous RLC phosphorylation is a crucial determinant of the Ca2+sensitivity of force development. Studies of the effects of RLC phosphorylation on the kinetics of force activation with the caged Ca2+, DM-nitrophen, showed a slight increase in the rates of force development with low statistical significance. However, an increase from 69 to 84% of the initial steady-state force was observed when nonphosphorylated RLC-reconstituted fibers were subsequently phosphorylated with exogenous myosin light chain kinase. In conclusion, our results suggest that, although Ca2+binding to the troponin-tropomyosin complex is the primary regulator of skeletal muscle contraction, RLC play an important modulatory role in this process.

Роль оксида азота в реализации антиоксидантного эффекта неопиатного аналога лей-энкефалина в сердце новорожденных белых крыс

2019 ◽  
pp. 61-64
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Postnatal Period ◽  
Oxide System ◽  
No Synthase ◽  
Albino Rats ◽  
Oxygen Species ◽  
Control Parameters ◽  
Synthase Inhibitor

The eff ect of the non-opiate analog of leu-enkephalin (peptide NALE: Phe – D – Ala – Gly – Phe – Leu – Arg) on the reactive oxygen species generation in the heart of albino rats in the early postnatal period was studied. Peptide NALE was administered intraperitoneally in the dose of 100 μ/kg daily from 2 to 6 days of life. Reactive oxygen species generation was assessed by chemiluminescence in the heart homogenates of 7-day-old animals. Decreasing of reactive oxygen species generation nearly by 30 % and an increasing in antioxidant system activity by the 20-27 %, compared with the control parameters, were found. The antioxidant eff ect of peptide NALE is associated with the presence of the amino acid Arg in the structure of the peptide. An analogue of NALE peptide, devoid of Arg (peptide Phe – D – Ala – Gly – Phe – Leu – Gly), had a signifi cant lower antioxidant eff ect. The NO-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in the dose 50 mg/kg, administered with NALE peptide, reduced the severity of the NALE antioxidant eff ect. The results of the study suggest that the pronounced antioxidant eff ect of NALE peptide in the heart of albino rats, at least in part, is due to the interaction with the nitric oxide system.

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