scholarly journals H-Wave® induces arteriolar vasodilation in rat striated muscle via nitric oxide-mediated mechanisms

2009 ◽  
Vol 27 (9) ◽  
pp. 1248-1251 ◽  
Author(s):  
Thomas L. Smith ◽  
Kenneth Blum ◽  
Michael F. Callahan ◽  
Nicholas A. DiNubile ◽  
Thomas J.H. Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Striated Muscle ◽  
Arteriolar Vasodilation

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.

Differences in EDNO contribution to arteriolar diameters at rest and during functional dilation in striated muscle

1993 ◽  
Vol 265 (1) ◽  
pp. H146-H151 ◽  
Author(s):  
R. L. Hester ◽  
A. Eraslan ◽  
Y. Saito
Keyword(s):  
Striated Muscle ◽  
Physiological Role ◽  
Second Order ◽  
Muscle Stimulation ◽  
Third Order ◽  
First Order ◽  
Before And After ◽  
Arteriolar Vasodilation ◽  
Arteriolar Diameter

This study was designed to determine the physiological role of endothelium-dependent nitric oxide (EDNO) in the control of arteriolar diameter during rest and muscle stimulation. Diameters of first-, second-, and third-order arterioles in the superfused hamster cremaster muscle were measured before and throughout 1 min of field stimulation before and after inhibition of EDNO release. ENDO inhibition by intravenous N omega-nitro-L-arginine methyl ester (L-NAME) significantly attenuated the arteriolar vasodilation in response to 1 microM acetylcholine. First-order arterioles averaged 65 +/- 5 microns at rest and dilated to 86 +/- 6 microns during muscle stimulation (n = 9), second-order arterioles averaged 45 +/- 6 microns and dilated to 72 +/- 3 microns during muscle stimulation (n = 6), with third-order arterioles averaging 29 +/- 2 microns, and dilating to 53 +/- 3 microns during muscle stimulation (n = 7). EDNO inhibition significantly decreased both the resting diameter of first-order arterioles (57 +/- 4 microns) and functional dilation (68 +/- 3 microns; P <0.05). EDNO inhibition had no effect on the resting diameter of second-order arterioles (45 +/- 5 microns) yet significantly attenuated the functional dilation (64 +/- 4 microns; P < 0.05). EDNO inhibition had no effect on either the resting diameter of third-order arterioles (30 +/- 2 microns) or the functional dilation (49 +/- 2 microns).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Direct Regulation of Striated Muscle Myosins by Nitric Oxide and Endogenous Nitrosothiols

PLoS ONE ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. e11209 ◽  
Author(s):  
Alicia M. Evangelista ◽  
Vijay S. Rao ◽  
Ashley R. Filo ◽  
Nadzeya V. Marozkina ◽  
Allan Doctor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Striated Muscle ◽  
Direct Regulation

NITRIC OXIDE SYNTHASE IN THE HETEROGENEOUS POPULATION OF INTRAMURAL STRIATED MUSCLE FIBRES OF THE HUMAN MEMBRANOUS URETHRAL SPHINCTER

1998 ◽  
Vol 159 (3) ◽  
pp. 1091-1096 ◽  
Author(s):  
KOSSEN M.T. HO ◽  
GORDON MCMURRAY ◽  
ALISON F. BRADING ◽  
JEREMY G. NOBLE ◽  
LARS NY ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Striated Muscle ◽  
Heterogeneous Population ◽  
Muscle Fibres ◽  
Urethral Sphincter ◽  
Oxide Synthase

Shear-dependent release of venular nitric oxide: effect on arteriolar tone in rat striated muscle

1996 ◽  
Vol 271 (2) ◽  
pp. H387-H395 ◽  
Author(s):  
M. A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Shear Rate ◽  
Striated Muscle ◽  
No Synthase ◽  
No Production ◽  
Contracting Muscle ◽  
Divergent Flow ◽  
Synthase Inhibitor ◽  
Arteriolar Tone ◽  
Resting Muscle

This study was designed to determine whether shear-dependent changes in venular nitric oxide (NO) production can influence nearby arteriolar tone and whether this mechanism contributes to functional arteriolar dilation in contracting muscle. In resting spinotrapezius muscle of anesthetized rats, occlusion of one branch of an arcade venular bifurcation with divergent flow caused flow and wall shear rate in the parallel branch to increase by an average of 99 and 72%, respectively. After 10–30 s, the paired arcade arteriole dilated by an average of 30%, with a correlation between the increase in venular shear rate and the magnitude of arteriolar dilation. During muscle contraction, arcade arterioles dilated by 73–97% and arcade venular shear rate increased by 48–83%. The NO synthase inhibitor NG-monomethyl-L-arginine greatly attenuated arteriolar dilation to increased venular shear rate in resting muscle but did not affect arteriolar dilation in contracting muscle. These findings suggest that a shear-dependent increase in venular NO release can dilate nearby arterioles, but this mechanism is not important for the sustained dilation of these arterioles during functional hyperemia.

Species-independent expression of nitric oxide synthase in the sarcolemma region of visceral and somatic striated muscle fibers

1995 ◽  
Vol 281 (3) ◽  
pp. 493-499 ◽  
Author(s):  
Zarko Grozdanovic ◽  
Georgios Nakos ◽  
Gudrun Dahrmann ◽  
Bernd Mayer ◽  
Reinhart Gossrau
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Striated Muscle ◽  
Muscle Fibers ◽  
Striated Muscle Fibers ◽  
Oxide Synthase

Effect of dietary salt on arteriolar nitric oxide in striated muscle of normotensive rats

1993 ◽  
Vol 264 (6) ◽  
pp. H1810-H1816 ◽  
Author(s):  
M. A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Striated Muscle ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake ◽  
Low Salt ◽  
Induced Hypertension

This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4–5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.

Nebivolol-induced vasodilation of renal afferent arterioles involves β3-adrenergic receptor and nitric oxide synthase activation

2012 ◽  
Vol 303 (5) ◽  
pp. F775-F782 ◽  
Author(s):  
Ming-Guo Feng ◽  
Minolfa C. Prieto ◽  
L. Gabriel Navar
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Soluble Guanylate Cyclase ◽  
Adrenergic Blocker ◽  
Afferent Arterioles ◽  
Renal Microvasculature ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Arteriolar Vasodilation

Nebivolol is a β1-adrenergic blocker that also elicits renal vasodilation and increases the glomerular filtration rate (GFR). However, its direct actions on the renal microvasculature and vasodilator mechanism have not been established. We used the in vitro blood-perfused juxtamedullary nephron technique to determine the vasodilator effects of nebivolol and to test the hypothesis that nebivolol induces vasodilation of renal afferent arterioles via an nitric oxide synthase (NOS)/nitric oxide (NO)/soluble guanylate cyclase (sGC)/cGMP pathway and the afferent arteriolar vasodilation effect may be mediated through the release of NO by activation of NOS via a β3-adrenoceptor-dependent mechanism. Juxtamedullary nephrons were superfused with nebivolol either alone or combined with the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or the NOS inhibitor Nω-nitro-l-arginine (l-NNA) or the β-blockers metoprolol (β1), butoxamine (β2), and SR59230A (β3). Nebivolol (100 μmol/l) markedly increased afferent and efferent arteriolar diameters by 18.9 ± 3.0 and 15.8 ± 1.8%. Pretreatment with l-NNA (1,000 μmol/l) or ODQ (10 μmol/l) decreased afferent vasodilator diameters and prevented the vasodilator effects of nebivolol (2.0 ± 0.2 and 2.4 ± 0.6%). Metoprolol did not elicit significant changes in afferent vasodilator diameters and did not prevent the effects of nebivolol to vasodilate afferent arterioles. However, treatment with SR59230A, but not butoxamine, markedly attenuated the vasodilation responses to nebivolol. Using a monoclonal antibody to β3-receptors revealed predominant immunostaining on vascular and glomerular endothelial cells. These data indicate that nebivolol vasodilates both afferent and efferent arterioles and that the afferent vasodilator effect is via a mechanism that is independent of β1-receptors but is predominantly mediated via a NOS/NO/sGC/cGMP-dependent mechanisms initiated by activation of endothelial β3-receptors.

scholarly journals Nitric Oxide - Its Importance in Swallowing, Inflammatory Bowel Disease and Cirrhotic Cardiomyopathy

2001 ◽  
Vol 15 (8) ◽  
pp. 551-552
Author(s):  
ABR Thomson
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Smooth Muscle ◽  
Esophageal Motility ◽  
Striated Muscle ◽  
Central Control ◽  
Solitary Tract ◽  
Esophageal Peristalsis ◽  
Primary Peristalsis

Nitric oxide is a neurotransmitter found in the central and peripheral nervous systems. Nitric oxide synthase (NOS) is localized in the central nervous system, including the nucleus of the solitary tract, nucleus ambiguus and dorsal motor nucleus of the vagus. These are regions that are implicated in the central control of swallowing and esophageal motility. In rats and rabbits, NOS has been shown to be present in the nucleus subcentralis of the nucleus of the solitary tract, and is thought to be responsible for the central programming of the striated muscle component of esophageal peristalsis. Beyak and co-workers from the University of Toronto, Toronto, Ontario provided evidence that the L-arginine-nitric oxide pathway is implicated in the central control of swallowing and esophageal motility. They studied oropharyngeal swallowing as well as esophageal peristalsis, and determined the functional role of brain stem nitric oxide by examining the effects of blockade of central nervous system NOS on swallowing, and on primary and secondary peristalsis. Administering NOS inhibitors intravenously or intracerebroventricularly into the fourth ventricle produced a number of oropharyngeal swallows and induced primary peristalsis in the smooth muscle portion of the esophageal body. NOS reduced the number of oropharyngeal swallows and the incidence of primary peristalsis in both smooth and striated muscle, and reduced the amplitude of peristalsis and smooth muscle contraction. This suggests that nitric oxide is a functional neurotransmitter in the central pattern generator responsible for swallowing and the central control of esophageal peristalsis. Peripherally administered NOS inhibitor can access structures within the blood-brain barrier to affect neuronal activity and physiological function. The central pattern generated for swallowing and esophageal peristalsis is suggested to be a serial network of linked neurons within the nucleus of the solitary tract and neighbouring reticular formation, and there is likely one subnetwork for the oropharyngeal phase and the other for the esophageal phase of swallowing. The neurosubstances mediating striated and smooth muscle peristalsis may be both anatomically and neurochemically distinct. The role of nitric oxide in the pathogenesis of esophageal motility disorders remains to be established.

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