Nitric Oxide as Possible Regulator of Energy-Dependent Ca2+ Transport in Mitochondria of Uterine Smooth Muscle

Author(s):  
Yuriy V. Danylovych ◽  
O. V. Kolomiets ◽  
G. V. Danylovych ◽  
Sergiy O. Kosterin
2014 ◽  
Vol 60 (2) ◽  
pp. 12-17 ◽  
Author(s):  
IuV Danylovych ◽  
◽  
OV Kolomiiets' ◽  
HV Danylovych ◽  
SO Kosterin ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Prosper A. Dabiré ◽  
Youssoufou Ouédraogo ◽  
Abel A. Somé ◽  
Stanislas Sawadogo ◽  
Issaka Ouédraogo ◽  
...  

In uterine smooth muscle, the effects of Excoecaria grahamii are not yet documented. To fill this gap, we investigated the pharmacological effect of Excoecaria grahamii on the contraction of the rat isolated uterine horns. The isolated segments were exposed to different concentrations of the aqueous extract of Excoecaria grahamii leaves and pharmacological drugs. The results showed that Excoecaria grahamii aqueous extract decreased the amplitude and frequency by concentration-related manner. I C 50 values were 2.4 and 2.6, respectively, for amplitude and frequency. Our study revealed that the extract did not act through histamine H2-receptors or the nitric oxide pathway. It also inhibited uterine contractions induced by oxytocin and potassium chloride (KCl). These data suggest that Excoecaria grahamii active compound can be used for calming uterine contractions. The action of Excoecaria grahamii showed that it can be useful to fight against diseases which caused uterotonic effects. It can be useful to prevent preterm birth and pains caused by menstruations but further investigation is needed to clarify the mechanism action.


1997 ◽  
Vol 272 (6) ◽  
pp. E1008-E1015 ◽  
Author(s):  
R. K. Riemer ◽  
C. Buscher ◽  
R. K. Bansal ◽  
S. M. Black ◽  
Y. He ◽  
...  

Nitric oxide (NO) relaxes uterine smooth muscle and is produced by the pregnant uterus. Our previous studies revealed an increase in rat uterine NO synthase (NOS) activity in pregnancy and a decline at term. In the present study, we have examined the distribution of NOS isoform expression to determine whether their regulation is consistent with a role in the inhibition of uterine contractions before term. At day 17-18 of pregnancy, NOS immunohistochemistry revealed expression of two isoforms: endothelial constitutive form of NOS (ecNOS) in vascular endothelium and inducible form of NOS (iNOS) in myometrial and vascular smooth muscle and in decidual epithelium. Immunoblotting revealed that expression of iNOS declined nearly fivefold, whereas ecNOS declined twofold in laboring rats at term. We conclude that iNOS is expressed in myometrium of pregnant rat uterus but not the virgin rat and that iNOS expression declines at term when labor is present. The pattern of changes in myometrial iNOS expression with advancing gestation suggests that NO could act in an autocrine and/or paracrine manner to inhibit uterine contractions before term.


2013 ◽  
Vol 305 (8) ◽  
pp. C803-C816 ◽  
Author(s):  
Craig Ulrich ◽  
David R. Quilici ◽  
Karen A. Schlauch ◽  
Iain L. O. Buxton

Molecular mechanisms involved in uterine quiescence during gestation and those responsible for induction of labor at term are incompletely known. More than 10% of babies born worldwide are premature and 1,000,000 die annually. Preterm labor results in preterm delivery in 50% of cases in the United States explaining 75% of fetal morbidity and mortality. There is no Food and Drug Administration-approved treatment to prevent preterm delivery. Nitric oxide-mediated relaxation of human uterine smooth muscle is independent of global elevation of cGMP following activation of soluble guanylyl cyclase. S-nitrosation is a likely mechanism to explain cGMP-independent relaxation to nitric oxide and may reveal S-nitrosated proteins as new therapeutic targets for the treatment of preterm labor. Employing S-nitrosoglutathione as an nitric oxide donor, we identified 110 proteins that are S-nitrosated in 1 or more states of human pregnancy. Using area under the curve of extracted ion chromatograms as well as normalized spectral counts to quantify relative expression levels for 62 of these proteins, we show that 26 proteins demonstrate statistically significant S-nitrosation differences in myometrium from spontaneously laboring preterm patients compared with nonlaboring patients. We identified proteins that were up- S-nitrosated as well as proteins that were down- S-nitrosated in preterm laboring tissues. Identification and relative quantification of the S-nitrosoproteome provide a fingerprint of proteins that can form the basis of hypothesis-directed efforts to understand the regulation of uterine contraction-relaxation and the development of new treatment for preterm labor.


2001 ◽  
Vol 185 (6) ◽  
pp. S214
Author(s):  
Yuri Vedernikov ◽  
Eva Fulep ◽  
George Saade ◽  
Robert Garfield

Life Sciences ◽  
1996 ◽  
Vol 58 (13) ◽  
pp. PL249-PL255 ◽  
Author(s):  
Yutaka Nakaya ◽  
Satoshi Yamamoto ◽  
Yoko Hamada ◽  
Masaharu Kamada ◽  
Toshihiro Aono ◽  
...  

1997 ◽  
Vol 238 (1) ◽  
pp. 12-16 ◽  
Author(s):  
Satoshi Yamamoto ◽  
Masaharu Kamada ◽  
Masahiko Maegawa ◽  
Masaya Takikawa ◽  
Yutaka Nakaya ◽  
...  

1998 ◽  
Vol 30 (1) ◽  
pp. 25-29 ◽  
Author(s):  
J.R. Pérez Vallina ◽  
L. Menéndez Antolin ◽  
B. Cantabrana ◽  
M. Sánchez ◽  
A. Hidalgo

1995 ◽  
Vol 74 (03) ◽  
pp. 980-986 ◽  
Author(s):  
Valérie B Schini-Kerth ◽  
Beate Fißithaler ◽  
Thomas T Andersen ◽  
John W Fenton ◽  
Paul M Vanhoutte ◽  
...  

SummaryProteolytically active forms of thrombin (α- and γ-thrombin) and thrombin receptor peptides inhibited the release of nitrite, a stable endproduct of nitric oxide, evoked by interleukin-1 β(IL-1 β) in cultured vascular smooth muscle cells while proteolytically inactive forms [D-Phe-Pro-Arg chloromethyl ketone-α-thrombin (PPACK-α- thrombin) and diisopropylphosphoryl-α-thrombin (DIP-α-thrombin)] had either no or only minimal inhibitory effects. Under bioassay conditions, perfusates from columns containing IL-1 β-activated vascular smooth muscle cells or cells treated with IL-1βplus PPACK-α-thrombin relaxed detector blood vessels. These relaxations were abolished by the inhibitor of nitric oxide synthesis, NG-nitro-L arginine. No relaxations were obtained with untreated cells or IL-1 β-treated cells in the presence of α-thrombin. The expression of inducible nitric oxide synthase mRNA and protein in vascular smooth muscle cells by IL-1 β was impaired by α-thrombin. These results demonstrate that thrombin regulates the expression of the inducible nitric oxide synthase at a transcriptional level via the proteolytic activation of the thrombin receptor in vascular smooth muscle cells


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