Evidence For The Existence Of A Constitutive Nitric Oxide Synthase In Vascular Smooth Muscle

Cheah, L. S.; Gwee, M.C.E.; Das, R; Ballard, HJ; Yang, Yagai; Daniel, E. E.; Kwan, C. Y.

doi:10.1046/j.1440-1681.2002.03707.x

Cited by 20 publications

(14 citation statements)

References 3 publications

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“…This suggests that NO responsible for the tachyphylaxis in EÀ rings is likely produced by a constitutive nNOS present in vascular smooth muscle cells. Our results confirm the study of Cheah et al (2002), which demonstrated a constitutive neuronal isoform of NOS present in vascular smooth muscle cells of Sprague-Dawley rats.…”

Section: Discussionsupporting

confidence: 91%

Role of nitric oxide and protein kinase C in the tachyphylaxis to vasopressin in rat aortic rings

2005

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Section: Discussionsupporting

confidence: 91%

Role of nitric oxide and protein kinase C in the tachyphylaxis to vasopressin in rat aortic rings

2005

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“…In blocking the production of NO from skeletal muscle, both endothelial cell and/or vascular smooth muscle cell production would also be blocked. The ability of endothelial cells to produce NO is well documented, and there is evidence that vascular smooth muscle cells contain NOS (9,10,12) and are capable of producing NO (10), although the purpose of this autocrine process is not well understood.…”

Section: Vasodilators Implicated In the Dilatory Response To Muscle Cmentioning

confidence: 99%

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

Dua¹,

Dua²,

Murrant³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Dua AK, Dua N, Murrant CL. Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency. Am J Physiol Heart Circ Physiol 297: H433-H442, 2009. First published May 22, 2009 doi:10.1152/ajpheart.00216.2009.-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 . 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. stimulus frequency; contraction frequency; arteriole; skeletal muscle contraction; active hyperemia BLOOD FLOW TO ACTIVE SKELETAL muscle increases during contraction. It is hypothesized that active skeletal muscle cell metabolites are a source of vasodilators that cause active hyperemia during contraction, but there is little consensus as to the identity of the vasodilators involved. A host of potential metabolic vasodilators such as adenosine (ADO), hydrogen ions, decreased oxygen tension, carbon dioxide, phosphate, etc., as well as a host of endothelial-derived products and products of muscle activation such as nitric oxide (NO), potassium (K ϩ ), prostaglandins, ACh, ATP-dependent K ϩ (K ATP ) channels, etc. (for review, see Refs. 6,18,28,36), have been implicated in the processes of active hyperemia, but there is a general lack of agreement as to the relative importance of each. We have been investigating the impact of stimulation parameters in the processes of arteriolar vasodilation during active hyperemia to understand this general lack of agreement. We surmised that if the dilators are proposed to be products of skeletal muscle activation or metabolism then it stands to reason that if activation or metabolism is changed through different stimulation parameters then the dilators being produced may also change. Thus, to understand the impact that stimulation parameters have on the production of different vasodilators in active hyperemia, we have investigated the effects of stimulation par...

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“…However, because the experiments were carried out in the presence of 1 M propranolol to eliminate any effect of norepinephrine on ␤-adrenoceptors, another more likely explanation may exist. Cheah et al (8) reported an electrical field stimulation/Ni 2ϩ / Mg 2ϩ -induced vasorelaxation in precontracted endotheliumdenuded rat aortic rings and vasorelaxation mediated through activation of nNOS in the vascular smooth muscle cells. Data from other studies also indicate the existence of nNOS in vascular smooth muscle cells (6,12).…”

Section: Norepinephrine Contraction During Hbo Exposurementioning

confidence: 99%

Vascular reactivity and endothelial NOS activity in rat thoracic aorta during and after hyperbaric oxygen exposure

Hink¹,

Thom²,

Simonsen³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Vascular reactivity and endothelial NOS activity in rat thoracic aorta during and after hyperbaric oxygen exposure. Am J Physiol Heart Circ Physiol 291: H1988 -H1998, 2006. First published April 28, 2006 doi:10.1152/ajpheart.00145.2006.-Accumulating evidence suggests that hyperbaric oxygen (HBO) stimulates neuronal nitric oxide (NO) synthase (NOS) activity, but the influence on endothelial NOS (eNOS) activity and vascular NO bioavailability remains unclear. We used a bioassay employing rat aortic rings to evaluate vascular NO bioavailability. HBO exposure to 2.8 atm absolute (ATA) in vitro decreased ACh relaxation. This effect remained unchanged, despite treatment with SOD-polyethylene glycol and catalase-polyethylene glycol, suggesting that the reduction in endothelium-derived NO bioavailability was independent of superoxide production. In vitro HBO induced contraction of resting aortic rings with and without endothelium, and these contractions were reduced by the NOS inhibitor N -nitro-L-arginine. In addition, in vitro HBO attenuated the vascular contraction produced by norepinephrine, and this effect was reversed by N -nitro-L-arginine, but not by endothelial denudation. These findings indicate stimulation of extraendothelial NO production during HBO exposure. A radiochemical assay was used to assess NOS activity in rat aortic endothelial cells. Catalytic activity of eNOS in cell homogenates was not decreased by HBO, and in vivo HBO exposure to 2.8 ATA was without effect on eNOS activity and/or vascular NO bioavailability in vitro. We conclude that HBO reduces endothelium-derived NO bioavailability independent of superoxide production, and this effect seems to be unrelated to a decrease in eNOS catalytic activity. In addition, HBO increases the resting tone of rat aortic rings and attenuates the contractile response to norepinephrine by endothelium-independent mechanisms that involve extraendothelial NO production. nitric oxide synthase; acetylcholine relaxation; autooxidation HYPERBARIC OXYGEN (HBO) is used in clinical medicine in the management of different diseases and conditions, because it mediates some useful actions, such as stimulation of angiogenesis and inhibition of leukocyte adhesion. However, the underlying biochemical mechanisms have not been fully elucidated.Nitric oxide (NO) bioavailability in rat and mouse cerebral cortex, measured by NO-specific microelectrodes, is increased early during HBO exposure and paralleled by an increase in regional blood flow (40). Thom et al. (40) reported that cerebral NO production was increased much more in knockout mice lacking genes for endothelial NO synthase (eNOS) than in those lacking genes for neuronal NO synthase (nNOS), suggesting that changes in eNOS activity during HBO exposure are minimal compared with changes in nNOS activity. However, because of the predominance of nNOS in the central nervous system (20), this might not be the case in the systemic circulation. Increased nNOS-but not eNOS-derived NO was also observed at the abluminal side of th...

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Evidence For The Existence Of A Constitutive Nitric Oxide Synthase In Vascular Smooth Muscle

Cited by 20 publications

References 3 publications

Role of nitric oxide and protein kinase C in the tachyphylaxis to vasopressin in rat aortic rings

Role of nitric oxide and protein kinase C in the tachyphylaxis to vasopressin in rat aortic rings

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

Vascular reactivity and endothelial NOS activity in rat thoracic aorta during and after hyperbaric oxygen exposure

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