Nitric Oxide Hyperpolarizes Arterial Smooth Muscle

1991 ◽  
Vol 17 (Supplement) ◽  
pp. 108???112 ◽  
Author(s):  
M. Tare ◽  
H. C. Parkington ◽  
H. A. Coleman ◽  
T. O. Neild ◽  
G. J. Dusting
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Arterial Smooth Muscle

Nitric oxide hyperpolarizes and relaxes uterine arterial smooth muscle

1990 ◽  
Vol 183 (4) ◽  
pp. 1608-1609
Author(s):  
M. Tare ◽  
H.C. Parkington ◽  
H.A. Coleman ◽  
T.O. Neild ◽  
G.J. Dusting
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Arterial Smooth Muscle

Hyperpolarization and relaxation of arterial smooth muscle caused by nitric oxide derived from the endothelium

Nature ◽  
1990 ◽  
Vol 346 (6279) ◽  
pp. 69-71 ◽  
Author(s):  
M. Tare ◽  
H. C. Parkington ◽  
H. A. Coleman ◽  
T. O. Neild ◽  
G. J. Dusting
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Arterial Smooth Muscle

scholarly journals Enhancement of myofilament calcium sensitivity by acute hypoxia in rat distal pulmonary arteries

2011 ◽  
Vol 301 (3) ◽  
pp. L380-L387 ◽  
Author(s):  
Letitia Weigand ◽  
Larissa A. Shimoda ◽  
J. T. Sylvester
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Acute Hypoxia ◽  
Rho Kinase ◽  
Mesenteric Arteries ◽  
Arterial Smooth Muscle ◽  
Force Relation ◽  
Endothelial Denudation ◽  
Pulmonary Arterial ◽  
Pulmonary Arterial Smooth Muscle

Hypoxic contraction of pulmonary arterial smooth muscle is thought to require increases in both intracellular Ca2+ concentration ([Ca2+]i) and myofilament Ca2+ sensitivity, which may or may not be endothelium-dependent. To examine the effects of hypoxia and endothelium on Ca2+ sensitivity in pulmonary arterial smooth muscle, we measured the relation between [Ca2+]i and isometric force at 37°C during normoxia (21% O2-5% CO2) and after 30 min of hypoxia (1% O2-5% CO2) in endothelium-intact (E+) and -denuded (E−) rat distal intrapulmonary arteries (IPA) permeabilized with staphylococcal α-toxin. Endothelial denudation enhanced Ca2+ sensitivity during normoxia but did not alter the effects of hypoxia, which shifted the [Ca2+]i-force relation to higher force in E+ and E− IPA. Neither hypoxia nor endothelial denudation altered Ca2+ sensitivity in mesenteric arteries. In E+ and E− IPA, hypoxic enhancement of Ca2+ sensitivity was abolished by the nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester (30 μM), which shifted normoxic [Ca2+]i-force relations to higher force. In E− IPA, the Rho kinase antagonist Y-27632 (10 μM) shifted the normoxic [Ca2+]i-force relation to lower force but did not alter the effects of hypoxia. These results suggest that acute hypoxia enhanced myofilament Ca2+ sensitivity in rat IPA by decreasing nitric oxide production and/or activity in smooth muscle, thereby revealing a high basal level of Ca2+ sensitivity, due in part to Rho kinase, which otherwise did not contribute to Ca2+ sensitization by hypoxia.

scholarly journals Intrauterine Nitric Oxide Deficiency Weakens Differentiation of Vascular Smooth Muscle in Newborn Rats

2021 ◽  
Vol 22 (15) ◽  
pp. 8003
Author(s):  
Anastasia A. Shvetsova ◽  
Anna A. Borzykh ◽  
Ekaterina K. Selivanova ◽  
Oxana O. Kiryukhina ◽  
Dina K. Gaynullina ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Early Ontogeny ◽  
Arterial Smooth Muscle ◽  
Pregnant Rats ◽  
Blood Concentrations ◽  
Myosin Heavy Chain Isoform ◽  
Nitric Oxide Deficiency ◽  
Cell Transcriptome ◽  
Synthase Inhibitor

Nitric oxide (NO) deficiency during pregnancy is a key reason for preeclampsia development. Besides its important vasomotor role, NO is shown to regulate the cell transcriptome. However, the role of NO in transcriptional regulation of developing smooth muscle has never been studied before. We hypothesized that in early ontogeny, NO is important for the regulation of arterial smooth muscle-specific genes expression. Pregnant rats consumed NO-synthase inhibitor L-NAME (500 mg/L in drinking water) from gestational day 10 till delivery, which led to an increase in blood pressure, a key manifestation of preeclampsia. L-NAME reduced blood concentrations of NO metabolites in dams and their newborn pups, as well as relaxations of pup aortic rings to acetylcholine. Using qPCR, we demonstrated reduced abundances of the smooth muscle-specific myosin heavy chain isoform, α-actin, SM22α, and L-type Ca2+-channel mRNAs in the aorta of newborn pups from the L-NAME group compared to control pups. To conclude, the intrauterine NO deficiency weakens gene expression specific for a contractile phenotype of arterial smooth muscle in newborn offspring.

scholarly journals Activation of Myosin Light Chain Phosphatase in Intact Arterial Smooth Muscle During Nitric Oxide-induced Relaxation

2001 ◽  
Vol 276 (37) ◽  
pp. 34681-34685 ◽  
Author(s):  
Elaine F. Etter ◽  
Masumi Eto ◽  
Robert L. Wardle ◽  
David L. Brautigan ◽  
Richard A. Murphy
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Myosin Light Chain Phosphatase ◽  
Arterial Smooth Muscle

Nitric oxide inhibits Ca2+ mobilization through cADP-ribose signaling in coronary arterial smooth muscle cells

2000 ◽  
Vol 279 (3) ◽  
pp. H873-H881 ◽  
Author(s):  
Jiang-Zhou Yu ◽  
David X. Zhang ◽  
Ai-Ping Zou ◽  
William B. Campbell ◽  
Pin-Lan Li
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Cyclase Activity ◽  
Arterial Smooth Muscle ◽  
Adp Ribosyl Cyclase ◽  
Intracellular Ca ◽  
Arterial Smooth Muscle Cells

The present study was designed to determine whether the cADP-ribose-mediated Ca2+ signaling is involved in the inhibitory effect of nitric oxide (NO) on intracellular Ca2+ mobilization. With the use of fluorescent microscopic spectrometry, cADP-ribose-induced Ca2+ release from sarcoplasmic reticulum (SR) of bovine coronary arterial smooth muscle cells (CASMCs) was determined. In the α-toxin-permeabilized primary cultures of CASMCs, cADP-ribose (5 μM) produced a rapid Ca2+ release, which was completely blocked by pretreatment of cells with the cADP-ribose antagonist 8-bromo-cADP-ribose (8-Br-cADPR). In intact fura 2-loaded CASMCs, 80 mM KCl was added to depolarize the cells and increase intracellular Ca2+ concentration ([Ca2+]i). Sodium nitroprusside (SNP), an NO donor, produced a concentration-dependent inhibition of the KCl-induced increase in [Ca2+]i, but it had no effect on the U-46619-induced increase in [Ca2+]i. In the presence of 8-Br-cADPR (100 μM) and ryanodine (10 μM), the inhibitory effect of SNP was markedly attenuated. HPLC analyses showed that CASMCs expressed the ADP-ribosyl cyclase activity, and SNP (1–100 μM) significantly reduced the ADP-ribosyl cyclase activity in a concentration-dependent manner. The effect of SNP was completely blocked by addition of 10 μM oxygenated hemoglobin. We conclude that ADP-ribosyl cyclase is present in CASMCs, and NO may decrease [Ca2+]i by inhibition of cADP-ribose-induced Ca2+ mobilization.

scholarly journals Arterial smooth muscle cells express nitric oxide synthase in response to endothelial injury.

1994 ◽  
Vol 180 (2) ◽  
pp. 733-738 ◽  
Author(s):  
G K Hansson ◽  
Y J Geng ◽  
J Holm ◽  
P Hårdhammar ◽  
A Wennmalm ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Endothelial Injury ◽  
No Production ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells ◽  
Oxide Synthase

Endothelial cells regulate vascular tone by secreting paracrine mediators that control the contractility of arterial smooth muscle cells. Nitric oxide (NO) is an important vasodilating agent that is generated from L-arginine by the enzyme nitric oxide synthase (NOS), which is expressed constitutively by the endothelium. NO also inhibits platelet aggregation, contributing to the antithrombotic properties of the endothelial surface. It would therefore be expected that loss of the endothelium during arterial injury would lead to vasospasm and thrombosis but instead, the neointima formed after injury has a nonthrombogenic surface and a maintained vascular patency. We report here that arterial smooth muscle cells in the neointima formed after a deendothelializing balloon injury to the rat carotid artery express the cytokine-inducible isoform of NOS. Expression was detectable by reverse transcription-polymerase chain reaction from day 1-14 after injury and in situ hybridization showed expression of NOS mRNA by neointimal smooth muscle cells, particularly at the surface of the lesion. This was associated with systemically detectable NO production as revealed by electron paramagnetic resonance spectroscopic analysis of nitrosylated red cell hemoglobin. Local NO production by intimal smooth muscle cells after endothelial injury could represent an important mechanism for the maintenance of arterial patency and nonthrombogenicity in the injured artery.

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