scholarly journals Pregnancy increases myometrial artery myogenic tone via NOS- or COX-independent mechanisms

2012 ◽  
Vol 303 (4) ◽  
pp. R368-R375 ◽  
Author(s):  
Delrae M. Eckman ◽  
Ridhima Gupta ◽  
Charles R. Rosenfeld ◽  
Timothy M. Morgan ◽  
Shelton M. Charles ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Pregnant Women ◽  
High Flow ◽  
Myogenic Tone ◽  
Internal Diameter ◽  
Pregnant Uterus ◽  
Voltage Dependent ◽  
Oxide Synthase ◽  
The Brain

Myogenic tone (MT) is a primary modulator of blood flow in the resistance vasculature of the brain, kidney, skeletal muscle, and perhaps in other high-flow organs such as the pregnant uterus. MT is known to be regulated by endothelium-derived factors, including products of the nitric oxide synthase (NOS) and/or the cyclooxygenase (COX) pathways. We asked whether pregnancy influenced MT in myometrial arteries (MA), and if so, whether such an effect could be attributed to alterations in NOS and/or COX. MA (200–300 μm internal diameter, 2–3 mm length) were isolated from 10 nonpregnant and 12 pregnant women undergoing elective hysterectomy or cesarean section, respectively. In the absence of NOS and/or COX inhibition, pregnancy was associated with increased MT in endothelium-intact MA compared with MA from nonpregnant women ( P < 0.01). The increase in MT was not due to increased Ca2+ entry via voltage-dependent channels since both groups of MA exhibited similar levels of constriction when exposed to 50 mM KCl. NOS inhibition ( Nω-nitro-l-arginine methyl ester, l-NAME) or combined NOS/COX inhibition (l-NAME/indomethacin) increased MT in MA from pregnant women ( P = 0.001 and P = 0.042, respectively) but was without effect in arteries from nonpregnant women. Indomethacin alone was without effect on MT in MA from either nonpregnant or pregnant women. We concluded that MT increases in MA during human pregnancy and that this effect was partially opposed by enhanced NOS activity.

Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action

Diabetes ◽  
1997 ◽  
Vol 46 (11) ◽  
pp. 1691-1700 ◽  
Author(s):  
S. Kapur ◽  
S. Bedard ◽  
B. Marcotte ◽  
C. H. Cote ◽  
A. Marette
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Insulin Action ◽  
Oxide Synthase

Localization of the cGMP-dependent protein kinases in relation to nitric oxide synthase in the brain

1999 ◽  
Vol 17 (1) ◽  
pp. 45-55 ◽  
Author(s):  
A.E.-D El-Husseini ◽  
J Williams ◽  
P.B Reiner ◽  
S Pelech ◽  
S.R Vincent
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protein Kinases ◽  
Dependent Protein ◽  
Oxide Synthase ◽  
The Brain

NO nerves in a tapeworm. NADPH-diaphorase histochemistry in adult Hymenolepis diminuta

Parasitology ◽  
1996 ◽  
Vol 113 (6) ◽  
pp. 559-565 ◽  
Author(s):  
M. K. S. Gustafsson ◽  
A. M. Lindholm ◽  
N. B. Terenina ◽  
M. Reuter
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nadph Diaphorase ◽  
Hymenolepis Diminuta ◽  
Staining Reaction ◽  
Internal Seminal Vesicle ◽  
Oxide Synthase ◽  
First Time ◽  
The Brain ◽  
Nerve Cords

SUMMARYThe free radical nitric oxide (NO), which is synthesized by nitric oxide synthase (NOS), has recently been discovered to function as a neuronal messenger. The presence of NOS was detected in the nervous system of adult Hymenolepis diminuta with NADPH-diaphorase (NADPH-d) histochemistry. The NADPH-d histochemical reaction is regarded as a selective marker for NOS in neuronal tissue. NADPH-d staining was observed in nerve fibres in the main and minor nerve cords and the transverse ring commissures, and in cell bodies in the brain commissure, along the main nerve cords, in the suckers and the rostellar sac. NADPH-d staining was also observed in the wall of the internal seminal vesicle and the genital atrium. The pattern of NADPH-d staining was compared with that of the 5-HT immunoreactive nervous elements. The NADPH-d staining reaction and the 5-HT immunoreactivity occur in separate sets of neurons. This is the first time the NADPH-d reaction has been demonstrated in the nervous system of a flatworm, indicating that NOS is present and that NO can be produced at this level of evolution.

scholarly journals Obesity, type 2 diabetes, and impaired insulin-stimulated blood flow: role of skeletal muscle NO synthase and endothelin-1

2017 ◽  
Vol 122 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Leryn J. Reynolds ◽  
Daniel P. Credeur ◽  
Camila Manrique ◽  
Jaume Padilla ◽  
Paul J. Fadel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Vastus Lateralis ◽  
Glucose Disposal ◽  
Endothelin 1 ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Increased endothelin-1 (ET-1) and reduced endothelial nitric oxide phosphorylation (peNOS) are hypothesized to reduce insulin-stimulated blood flow in type 2 diabetes (T2D), but studies examining these links in humans are limited. We sought to assess basal and insulin-stimulated endothelial signaling proteins (ET-1 and peNOS) in skeletal muscle from T2D patients. Ten obese T2D [glucose disposal rate (GDR): 6.6 ± 1.6 mg·kg lean body mass (LBM)−1·min−1] and 11 lean insulin-sensitive subjects (Lean GDR: 12.9 ± 1.2 mg·kg LBM−1·min−1) underwent a hyperinsulinemic-euglycemic clamp with vastus lateralis biopsies taken before and 60 min into the clamp. Basal biopsies were also taken in 11 medication-naïve, obese, non-T2D subjects. ET-1, peNOS (Ser1177), and eNOS protein and mRNA were measured from skeletal muscle samples containing native microvessels. Femoral artery blood flow was assessed by duplex Doppler ultrasound. Insulin-stimulated blood flow was reduced in obese T2D (Lean: +50.7 ± 6.5% baseline, T2D: +20.8 ± 5.2% baseline, P < 0.05). peNOS/eNOS content was higher in Lean under basal conditions and, although not increased by insulin, remained higher in Lean during the insulin clamp than in obese T2D ( P < 0.05). ET-1 mRNA and peptide were 2.25 ± 0.50- and 1.52 ± 0.11-fold higher in obese T2D compared with Lean at baseline, and ET-1 peptide remained 2.02 ± 1.9-fold elevated in obese T2D after insulin infusion ( P < 0.05) but did not increase with insulin in either group ( P > 0.05). Obese non-T2D subjects tended to also display elevated basal ET-1 ( P = 0.06). In summary, higher basal skeletal muscle expression of ET-1 and reduced peNOS/eNOS may contribute to a reduced insulin-stimulated leg blood flow response in obese T2D patients. NEW & NOTEWORTHY Although impairments in endothelial signaling are hypothesized to reduce insulin-stimulated blood flow in type 2 diabetes (T2D), human studies examining these links are limited. We provide the first measures of nitric oxide synthase and endothelin-1 expression from skeletal muscle tissue containing native microvessels in individuals with and without T2D before and during insulin stimulation. Higher basal skeletal muscle expression of endothelin-1 and reduced endothelial nitric oxide phosphorylation (peNOS)/eNOS may contribute to reduced insulin-stimulated blood flow in obese T2D patients.

scholarly journals Influence of Active Exposure to Tobacco Smoke on Nitric Oxide Status of Pregnant Women

2018 ◽  
Vol 15 (12) ◽  
pp. 2719 ◽  
Author(s):  
Magdalena Chełchowska ◽  
Jadwiga Ambroszkiewicz ◽  
Joanna Gajewska ◽  
Joanna Mazur ◽  
Leszek Lewandowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Pregnant Women ◽  
Smoking Status ◽  
Multivariate Regression Analysis ◽  
Smoking During Pregnancy ◽  
Women Subjects ◽  
Total Antioxidant ◽  
Markers Of Oxidative Stress ◽  
Oxide Synthase

Smoking tobacco can impair proper vascular endothelial functioning. This is exhibited through reduced nitric oxide synthesis as well as activity due to accompanying oxidative stress. We examined the relationship between nitric oxide and markers of oxidative stress/antioxidant defense in serum of smoking and non-smoking pregnant women. Subjects included 99 healthy pregnant women, who were tested for nitric oxide (NO), endothelial (eNOS) and inducible (iNOS) nitric oxide synthase, total oxidant capacity (TOC), and total antioxidant capacity (TAC). NO, eNOS, and TAC serum concentrations were significantly lower (p < 0.005), but iNOS (p < 0.05) and TOC (p < 0.001) were higher in smokers than in non-smokers. Multivariate regression analysis showed associations between NO concentration and eNOS, TAC, and smoking status in the whole group of patients. In the model estimated separately for smokers, the highest impact of eNOS (β = 0.375; p = 0.021) and cotinine (β = −0.323; p = 0.037) was indicated for NO concentration. In the model of non-smokers, eNOS (β = 0.291, p = 0.030) and TAC (β = 0.350; p = 0.015) were important for NO level. Smoking during pregnancy could exacerbate oxidative stress, impair the action of nitric oxide synthases, and adversely affect the balance of oxygen and nitrogen metabolism. Relationships between NO concentrations and TAC in the studied women’s blood can confirm the antioxidant nature of nitric oxide.

Effects of lipoproteins from pre-eclamptic women on umbilical endothelial cell 6-oxo-prostaglandin F1α and endothelin 1 synthesis, and nitric oxide synthase 3 mRNA expression

1999 ◽  
Vol 97 (6) ◽  
pp. 697-706 ◽  
Author(s):  
A. BARDEN ◽  
L. J. BEILIN ◽  
K. BOTH ◽  
J. RITCHIE ◽  
P. LEEDMAN ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Pregnant Women ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Endothelin 1 ◽  
Nitric Oxide Synthase 3 ◽  
Oxide Synthase

In order to evaluate whether lipid abnormalities may contribute to endothelial dysfunction in pre-eclampsia, the present study examined the in vitro effects of very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL), isolated from women with pre-eclampsia and matched controls, on the endothelial synthesis of 6-oxo-prostaglandin F1α (6-oxo-PGF1α; a metabolite of prostacyclin) and endothelin 1, and on the expression of nitric oxide synthase 3 (NOS3) mRNA. VLDL, LDL and HDL cholesterol were isolated from 20 pre-eclamptic and 20 age- and gestation-matched normal pregnant women. The lipoproteins (50 μg/ml) and lipoprotein-free control plasma were incubated for 1, 3 and 6 h at 37 °C with a human umbilical endothelial cell line. The synthesis of 6-oxo-PGF1α and endothelin 1, and NOS3 mRNA expression, were measured at each time point. VLDL from pre-eclamptic women stimulated endothelial cell 6-oxo-PGF1α synthesis to a lesser extent than that from normal pregnant women (P< 0.05). LDL from women with pre-eclampsia also stimulated 6-oxo-PGF1α synthesis to a lesser extent than LDL from normal pregnant women, but the effect was less sustained. The effect of HDL from women with pre-eclampsia on 6-oxo-PGF1α synthesis was similar to that of HDL from normal pregnant women. The pre-incubation levels of lipid peroxides in VLDL and LDL were not different between the normal pregnant and pre-eclamptic women, and cannot account for the decrease in 6-oxo-PGF1α synthesis. VLDL, LDL and HDL from women with pre-eclampsia did not affect endothelial cell synthesis of endothelin 1 or expression of NOS3 mRNA differently from lipoproteins from normal pregnant women. This study suggests that VLDL, and to a lesser extent LDL, from women with pre-eclampsia could potentially contribute to the reduced systemic 6-oxo-PGF1α synthesis observed in the pre-eclamptic syndrome.

Glucose uptake during contraction in isolated skeletal muscles from neuronal nitric oxide synthase μ knockout mice

2015 ◽  
Vol 118 (9) ◽  
pp. 1113-1121 ◽  
Author(s):  
Yet Hoi Hong ◽  
Tony Frugier ◽  
Xinmei Zhang ◽  
Robyn M. Murphy ◽  
Gordon S. Lynch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Organ Bath ◽  
Skeletal Muscle Glucose Uptake ◽  
Nos Inhibitor ◽  
Amp Activated Protein Kinase ◽  
Oxide Synthase

Inhibition of nitric oxide synthase (NOS) significantly attenuates the increase in skeletal muscle glucose uptake during contraction/exercise, and a greater attenuation is observed in individuals with Type 2 diabetes compared with healthy individuals. Therefore, NO appears to play an important role in mediating muscle glucose uptake during contraction. In this study, we investigated the involvement of neuronal NOSμ (nNOSμ), the main NOS isoform activated during contraction, on skeletal muscle glucose uptake during ex vivo contraction. Extensor digitorum longus muscles were isolated from nNOSμ−/−and nNOSμ+/+mice. Muscles were contracted ex vivo in a temperature-controlled (30°C) organ bath with or without the presence of the NOS inhibitor NG-monomethyl-l-arginine (L-NMMA) and the NOS substrate L-arginine. Glucose uptake was determined by radioactive tracers. Skeletal muscle glucose uptake increased approximately fourfold during contraction in muscles from both nNOSμ−/−and nNOSμ+/+mice. L-NMMA significantly attenuated the increase in muscle glucose uptake during contraction in both genotypes. This attenuation was reversed by L-arginine, suggesting that L-NMMA attenuated the increase in muscle glucose uptake during contraction by inhibiting NOS and not via a nonspecific effect of the inhibitor. Low levels of NOS activity (∼4%) were detected in muscles from nNOSμ−/−mice, and there was no evidence of compensation from other NOS isoform or AMP-activated protein kinase which is also involved in mediating muscle glucose uptake during contraction. These results indicate that NO regulates skeletal muscle glucose uptake during ex vivo contraction independently of nNOSμ.

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