Nitric Oxide (NO) Stimulates Gonadotropin Secretion in vitro through a Calcium-Dependent, cGMP-Independent Mechanism

1998 ◽  
Vol 68 (3) ◽  
pp. 180-186 ◽  
Author(s):  
Leonor Pinilla ◽  
Dolores González ◽  
Manuel Tena-Sempere ◽  
Enrique Aguilar
Keyword(s):  
Nitric Oxide ◽  
Gonadotropin Secretion ◽  
Calcium Dependent ◽  
Independent Mechanism

Regulation of human placental fetal vessel tone: role of nitric oxide

1995 ◽  
Vol 7 (6) ◽  
pp. 1407 ◽  
Author(s):  
RG King ◽  
NM Gude ◽  
Iulio JL Di ◽  
SP Brennecke
Keyword(s):  
Nitric Oxide ◽  
Perfusion Pressure ◽  
Factors Affecting ◽  
Endothelin 1 ◽  
Calcium Dependent ◽  
Fetal Vessel ◽  
Nitric Oxide Inhibitors ◽  
Vessel Resistance ◽  
Endothelin 3

Factors affecting fetal vessel resistance have been studied in vitro in bilaterally perfused lobules of human placentae. Potent and efficacious constrictors in this preparation (in order of potency) include endothelin-1 > the thromboxane mimetic U46619 > endothelin-3 > prostaglandin F2 alpha. Inhibitors of eicosanoid synthesis did not affect fetal vessel basal perfusion pressure, nor did they potentiate the effects of the vasoconstrictor U46619. In contrast, the nitric oxide inhibitors N omega-nitro-L-arginine (NOLA), haemoglobin and methylene blue all increased fetal vessel basal perfusion pressure and also increased U46619-induced constriction. Similarly, NOLA markedly potentiated the constrictor effects of endothelin-1, angiotensin II, 5-hydroxytryptamine and bradykinin. These studies therefore provide evidence that NO is important in the maintenance of low basal fetal vessel impedance and also reduces the effects of a number of vasoconstrictor autacoids. Nitric oxide synthase (NOS) activity of human placental homogenates has been measured and shown to be mainly calcium-dependent. Human placental NOS activity was not affected by labour state but was reduced in pre-eclampsia. No evidence was found that in pre-eclampsia raised concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine were responsible for the reduced placental NOS activity. Hence, these studies provide evidence that NO is an important endogenous dilator of the fetal vessels of the human placenta and that reduced NOS activity could contribute to the pathogenesis and/or effects of pre-eclampsia.

Calcium regulates estrogen increase in permeability of cultured CaSki epithelium by eNOS-dependent mechanism

2000 ◽  
Vol 279 (5) ◽  
pp. C1495-C1505 ◽  
Author(s):  
George I. Gorodeski
Keyword(s):  
Nitric Oxide ◽  
Endothelial Nitric Oxide Synthase ◽  
Cytosolic Calcium ◽  
No Synthase ◽  
Calcium Dependent ◽  
Steady State Levels ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Dependent Mechanism

Estrogen increases baseline transepithelial permeability across CaSki cultures and augments the increase in permeability in response to hypertonic gradients. In estrogen-treated cells, lowering cytosolic calcium abrogated the hypertonicity-induced augmented increase in permeability and decreased baseline permeability to a greater degree than in estrogen-deprived cells. Steady-state levels of cytosolic calcium in estrogen-deprived cells were higher than in estrogen-treated cells. Increases in extracellular calcium increased cytosolic calcium more in estrogen-deprived cells than in estrogen-treated cells. However, in estrogen-treated cells, increasing cytosolic calcium was associated with greater increases in permeability in response to hypertonic gradients than in estrogen-deprived cells. Lowering cytosolic calcium blocked the estrogen-induced increase in nitric oxide (NO) release and in the in vitro conversion of l-[3H]arginine to l-[3H]citrulline. Treatment with estrogen upregulated mRNA of the NO synthase isoform endothelial nitric oxide synthase (eNOS). These results indicate that cytosolic calcium mediates the responses to estrogen and suggest that the estrogen increase in permeability and the augmented increase in permeability in response to hypertonicity involve an increase in NO synthesis by upregulation of the calcium-dependent eNOS.

scholarly journals Direct stimulatory effect of ghrelin on pituitary release of LH through a nitric oxide-dependent mechanism that is modulated by estrogen

Reproduction ◽  
2007 ◽  
Vol 133 (6) ◽  
pp. 1223-1232 ◽  
Author(s):  
Rafael Fernández-Fernández ◽  
Manuel Tena-Sempere ◽  
Juan Roa ◽  
Juan Manuel Castellano ◽  
Víctor M Navarro ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reproductive Function ◽  
Female Rats ◽  
Experimental Conditions ◽  
Gonadotropin Secretion ◽  
Minimal Effective Dose ◽  
Gh Secretion ◽  
Lh Secretion

Ghrelin, a gut peptide with key actions on food intake and GH secretion, has been recently recognized as potential regulator of reproductive function. Thus, in adult female rats, ghrelin has been proven to modulate GnRH/LH secretion, with predominant inhibitory effectsin vivo. We analyze herein potential direct pituitary effects of ghrelin on basal and GnRH-stimulated gonadotropin secretion in prepubertal female rats, and its interplay with ovarian inputs, nitric oxide (NO), and hypothalamic differentiation. In the experimental setting, pituitaries from intact and ovariectomized prepubertal female rats were challenged with ghrelinin vitroand LH secretion was monitored. Our results demonstrate that 1) ghrelin consistently stimulatedin vitropituitary LH secretion under different experimental conditions; 2) the sensitivity to ghrelin, expressed either as the minimal effective dose or the amplitude of the LH response, was modulated by ovarian inputs; 3) the blockade of estrogen action significantly augmented the stimulatory effect of ghrelin; 4) the stimulatory effect of ghrelin on LH secretion required proper NO synthesis; and 5) the ability of ghrelin to elicit LH secretionin vitrowas preserved after alteration (masculinization) of brain sexual differentiation. Overall, our present data reinforce the concept that ghrelin participates in the control of LH secretion, with potential stimulatory actions at the pituitary level that require the presence of NO and are modulated by ovarian signals.

scholarly journals Tyrosine nitration on calmodulin enhances calcium-dependent association and activation of nitric-oxide synthase

2019 ◽  
Vol 295 (8) ◽  
pp. 2203-2211 ◽  
Author(s):  
Joseph J. Porter ◽  
Hyo Sang Jang ◽  
Mohammad Mahfuzul Haque ◽  
Dennis J. Stuehr ◽  
Ryan A. Mehl
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Calcium Binding ◽  
Vascular Dysfunction ◽  
Post Translational Modification ◽  
Calcium Dependent ◽  
Genetic Code Expansion ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Production of reactive oxygen species caused by dysregulated endothelial nitric-oxide synthase (eNOS) activity is linked to vascular dysfunction. eNOS is a major target protein of the primary calcium-sensing protein calmodulin. Calmodulin is often modified by the main biomarker of nitroxidative stress, 3-nitrotyrosine (nitroTyr). Despite nitroTyr being an abundant post-translational modification on calmodulin, the mechanistic role of this modification in altering calmodulin function and eNOS activation has not been investigated. Here, using genetic code expansion to site-specifically nitrate calmodulin at its two tyrosine residues, we assessed the effects of these alterations on calcium binding by calmodulin and on binding and activation of eNOS. We found that nitroTyr–calmodulin retains affinity for eNOS under resting physiological calcium concentrations. Results from in vitro eNOS assays with calmodulin nitrated at Tyr-99 revealed that this nitration reduces nitric-oxide production and increases eNOS decoupling compared with WT calmodulin. In contrast, calmodulin nitrated at Tyr-138 produced more nitric oxide and did so more efficiently than WT calmodulin. These results indicate that the nitroTyr post-translational modification, like tyrosine phosphorylation, can impact calmodulin sensitivity for calcium and reveal Tyr site-specific gain or loss of functions for calmodulin-induced eNOS activation.

scholarly journals Clearance of Shigella flexneri Infection Occurs through a Nitric Oxide-Independent Mechanism

1998 ◽  
Vol 66 (6) ◽  
pp. 3012-3016 ◽  
Author(s):  
Sing Sing Way ◽  
Marcia B. Goldberg
Keyword(s):  
Nitric Oxide ◽  
Shigella Flexneri ◽  
Intracellular Pathogens ◽  
Free System ◽  
Innate Resistance ◽  
Cell Free System ◽  
Independent Mechanism ◽  
A Cell ◽  
Ifn Γ

ABSTRACT Nitric oxide (NO) generated by gamma interferon (IFN-γ) activation of macrophages mediates the killing of many intracellular pathogens. IFN-γ is essential to innate resistance to Shigella flexneri infection. We demonstrate that NO is produced followingS. flexneri infection both in mice and in activated cells in vitro and that while it is able to kill S. flexneri in a cell-free system, it is not required for clearance of S. flexneri in either infected mice or in activated cells in vitro.

Bisphosphonates induce apoptosis in mouse macrophage-like cells in vitro by a nitric oxide-independent mechanism

2009 ◽  
Vol 11 (10) ◽  
pp. 1482-1491 ◽  
Author(s):  
Michael J. Rogers ◽  
Kattya M. Chilton ◽  
Fraser P. Coxon ◽  
John Lawry ◽  
M. Olivia Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mouse Macrophage ◽  
Independent Mechanism
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