scholarly journals Release of nitric oxide from glyceryl trinitrate by captopril but not enalaprilat: in vitro and in vivo studies

1993 ◽  
Vol 109 (2) ◽  
pp. 430-436 ◽  
Author(s):  
Daniela Salvemini ◽  
Alessandra Pistelli ◽  
Vincenzo Mollace
Keyword(s):  
Nitric Oxide ◽  
Glyceryl Trinitrate ◽  
In Vivo Studies

scholarly journals Novel Insights on the Role of Nitric Oxide in the Ovary: A Review of the Literature

2021 ◽  
Vol 18 (3) ◽  
pp. 980
Author(s):  
Maria Cristina Budani ◽  
Gian Mario Tiboni
Keyword(s):  
Nitric Oxide ◽  
In Vivo Studies ◽  
Published Data ◽  
Vitro Fertilization ◽  
Peripheral Neurons ◽  
Relevant Role ◽  
Oocyte Meiotic Maturation

Nitric oxide (NO) is formed during the oxidation of L-arginine to L-citrulline by the action of multiple isoenzymes of NO synthase (NOS): neuronal NOS (nNOS), endotelial NOS (eNOS), and inducible NOS (iNOS). NO plays a relevant role in the vascular endothelium, in central and peripheral neurons, and in immunity and inflammatory systems. In addition, several authors showed a consistent contribution of NO to different aspects of the reproductive physiology. The aim of the present review is to analyse the published data on the role of NO within the ovary. It has been demonstrated that the multiple isoenzymes of NOS are expressed and localized in the ovary of different species. More to the point, a consistent role was ascribed to NO in the processes of steroidogenesis, folliculogenesis, and oocyte meiotic maturation in in vitro and in vivo studies using animal models. Unfortunately, there are few nitric oxide data for humans; there are preliminary data on the implication of nitric oxide for oocyte/embryo quality and in-vitro fertilization/embryo transfer (IVF/ET) parameters. NO plays a remarkable role in the ovary, but more investigation is needed, in particular in the context of human ovarian physiology.

scholarly journals Reciprocal regulation of the nitric oxide and cyclooxygenase pathway in pathophysiology: relevance and clinical implications

2013 ◽  
Vol 304 (7) ◽  
pp. R473-R487 ◽  
Author(s):  
Daniela Salvemini ◽  
Sangwon F. Kim ◽  
Vincenzo Mollace
Keyword(s):  
Nitric Oxide ◽  
Arachidonic Acid ◽  
State Of The Art ◽  
No Synthase ◽  
In Vivo Studies ◽  
Clinical Implications ◽  
Reciprocal Regulation ◽  
Receptor Targets

The nitric oxide (NO) and cyclooxygenase (COX) pathways share a number of similarities. Nitric oxide is the mediator generated from the NO synthase (NOS) pathway, and COX converts arachidonic acid to prostaglandins, prostacyclin, and thromboxane A2. Two major forms of NOS and COX have been identified to date. The constitutive isoforms critically regulate several physiological states. The inducible isoforms are overexpressed during inflammation in a variety of cells, producing large amounts of NO and prostaglandins, which may underlie pathological processes. The cross-talk between the COX and NOS pathways was initially reported by Salvemini and colleagues in 1993, when they demonstrated in a series of in vitro and in vivo studies that NO activates the COX enzymes to produce increased amounts of prostaglandins. Those studies led to the concept that COX enzymes represent important endogenous “receptor” targets for amplifying or modulating the multifaceted roles of NO in physiology and pathology. Since then, numerous studies have furthered our mechanistic understanding of these interactions in pathophysiological settings and delineated potential clinical outcomes. In addition, emerging evidence suggests that the canonical nitroxidative species (NO, superoxide, and/or peroxynitrite) modulate biosynthesis of prostaglandins through non-COX-related pathways. This article provides a comprehensive state-of-the art overview in this area.

Production and functional roles of nitric oxide in the proximal tubule

2000 ◽  
Vol 278 (5) ◽  
pp. R1117-R1124 ◽  
Author(s):  
Mingyu Liang ◽  
Franklyn G. Knox
Keyword(s):  
Nitric Oxide ◽  
Proximal Tubule ◽  
In Vivo Studies ◽  
Sodium Reabsorption ◽  
Functional Roles ◽  
Enhanced Production ◽  
Proximal Tubular ◽  
Final Effect

A significant role for nitric oxide (NO) in proximal tubule physiology and pathophysiology has been revealed by a series of in vivo and in vitro studies. Whether the proximal tubule produces NO under basal conditions is still controversial; however, evidence suggests that the proximal tubule is constantly exposed to NO that might include NO from nonproximal tubule sources. When challenged with a variety of stimuli, including hypoxia, the proximal tubule is able to produce large quantities of NO. In vivo studies generally indicate that NO inhibits fluid and sodium reabsorption by the proximal tubule. However, the final effect of NO on proximal tubular reabsorption appears to depend on the concentration of NO and involve interaction with other regulatory mechanisms. NO regulates Na+-K+-ATPase, Na+/H+ exchangers, and paracellular permeability of proximal tubular cells, which may contribute to its effect on proximal tubular transport. Enhanced production of NO, perhaps depending on macrophage type inducible NO synthase, participates in hypoxic/ischemic proximal tubular injury. In conclusion, NO plays a fundamental role in both physiology and pathophysiology of the proximal tubule.

Inhaled nitric oxide induced NOS inhibition and rebound pulmonary hypertension: a role for superoxide and peroxynitrite in the intact lamb

2006 ◽  
Vol 290 (2) ◽  
pp. L359-L366 ◽  
Author(s):  
Peter Oishi ◽  
Albert Grobe ◽  
Eileen Benavidez ◽  
Boaz Ovadia ◽  
Cynthia Harmon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Inhaled Nitric Oxide ◽  
In Vivo Studies ◽  
Acute Increase ◽  
No Signaling ◽  
Oxide Synthase ◽  
Inhaled No

Previous in vivo studies indicate that inhaled nitric oxide (NO) decreases nitric oxide synthase (NOS) activity and that this decrease is associated with significant increases in pulmonary vascular resistance (PVR) upon the acute withdrawal of inhaled NO (rebound pulmonary hypertension). In vitro studies suggest that superoxide and peroxynitrite production during inhaled NO therapy may mediate these effects, but in vivo data are lacking. The objective of this study was to determine the role of superoxide in the decrease in NOS activity and rebound pulmonary hypertension associated with inhaled NO therapy in vivo. In control lambs, 24 h of inhaled NO (40 ppm) decreased NOS activity by 40% ( P < 0.05) and increased endothelin-1 levels by 64% ( P < 0.05). Withdrawal of NO resulted in an acute increase in PVR (60.7%, P < 0.05). Associated with these changes, superoxide and peroxynitrite levels increased more than twofold ( P < 0.05) following 24 h of inhaled NO therapy. However, in lambs treated with polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) during inhaled NO therapy, there was no change in NOS activity, no increase in superoxide or peroxynitrite levels, and no increase in PVR upon the withdrawal of inhaled NO. In addition, endothelial NOS nitration was 18-fold higher ( P < 0.05) in control lambs than in PEG-SOD-treated lambs following 24 h of inhaled NO. These data suggest that superoxide and peroxynitrite participate in the decrease in NOS activity and rebound pulmonary hypertension associated with inhaled NO therapy. Reactive oxygen species scavenging may be a useful therapeutic strategy to ameliorate alterations in endogenous NO signaling during inhaled NO therapy.

scholarly journals Effect of the nitric oxide donor, glyceryl trinitrate, on human gall bladder motility

Gut ◽  
1998 ◽  
Vol 42 (3) ◽  
pp. 410-413 ◽  
Author(s):  
R Greaves ◽  
J Miller ◽  
L O’Donnell ◽  
A McLean ◽  
M J G Farthing
Keyword(s):  
Nitric Oxide ◽  
Gall Bladder ◽  
Glyceryl Trinitrate ◽  
Bladder Volume ◽  
Nitric Oxide Donor ◽  
Fasting State ◽  
Double Blind ◽  
Bladder Emptying

Background—Nitric oxide is a major neurotransmitter in non-adrenergic, non-cholinergic (NANC) pathways. NANC inhibitory innervation has been shown in human gall bladder muscle in vitro; the role of nitric oxide in human gall bladder emptying however is undefined.Aims—To study the effect of glyceryl trinitrate, a nitric oxide donor, on gall bladder emptying in healthy subjects using a randomised, double blind, crossover, placebo controlled design.Methods—Ultrasonographic gall bladder volume was measured in the fasting state in eight healthy volunteers after randomised administration of either glyceryl trinitrate 1200 μg buccal spray or placebo spray. On two further occasions, after randomised administration of either glyceryl trinitrate 1200 μg buccal spray or placebo spray, gall bladder volumes were also measured after a liquid test meal.Results—Glyceryl trinitrate significantly increased fasting gall bladder volume to a mean of 114% (SEM 5%) of pretreatment volume (p=0.039). Glyceryl trinitrate also significantly impaired gall bladder emptying between five and 40 minutes postprandially. Gall bladder ejection fraction was also reduced after glyceryl trinitrate compared with placebo (43 (6.9)% versus 68.4 (6.5)%, p=0.016).Conclusions—This study shows that glyceryl trinitrate produces gall bladder dilatation in the fasting state and reduces postprandial gall bladder emptying, suggesting that nitric oxide mechanisms may be operative in the human gall bladder in vivo.

Hyperoxia induces retinal vascular endothelial cell apoptosis through formation of peroxynitrite

2003 ◽  
Vol 285 (3) ◽  
pp. C546-C554 ◽  
Author(s):  
Xiaolin Gu ◽  
Azza B. El-Remessy ◽  
Steven E. Brooks ◽  
Mohamed Al-Shabrawey ◽  
Nai-Tsi Tsai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cell ◽  
In Vivo Studies ◽  
Endothelial Cell Apoptosis ◽  
Akt Kinase ◽  
Induced Apoptosis

Hyperoxia exposure induces capillary endothelial cell apoptosis in the developing retina, leading to vaso-obliteration followed by proliferative retinopathy. Previous in vivo studies have shown that endothelial nitric oxide synthase (NOS3) and peroxynitrite are important mediators of the vaso-obliteration. Now we have investigated the relationship between hyperoxia, NOS3, peroxynitrite, and endothelial cell apoptosis by in vitro experiments using bovine retinal endothelial cells (BREC). We found that BREC exposed to 40% oxygen (hyperoxia) for 48 h underwent apoptosis associated with activation of caspase-3 and cleavage of the caspase substrate poly(ADP-ribose) polymerase. Hyperoxia-induced apoptosis was associated with increased formation of nitric oxide, peroxynitrite, and superoxide anion and was blocked by treatment with uric acid, nitro-l-arginine methyl ester, or superoxide dismutase. Analyses of the phosphatidylinositol 3-kinase/Akt kinase survival pathway in cells directly treated with peroxynitrite revealed inhibition of VEGF- and basic FGF-induced activation of Akt kinase. These results suggest that hyperoxia-induced formation of peroxynitrite induces BREC apoptosis by crippling key survival pathways and that blocking peroxynitrite formation prevents apoptosis. These data may have important clinical implications for infants at risk of retinopathy of prematurity.

scholarly journals The Immunomodulatory, Nitric Oxide and Cytokine activity of SeptilinTM

2019 ◽  
Vol 18 (4) ◽  
pp. 675-688
Author(s):  
Mujeeb Hoosen
Keyword(s):  
Nitric Oxide ◽  
Medical Science ◽  
Herbal Medicines ◽  
In Vivo Studies ◽  
Therapeutic Success ◽  
Herbal Products ◽  
Hand Search ◽  
Natural Medicine

Objective: Herbal immunomodulatory preparations are increasing in popularity. In vitro, in vivo and clinical trial studies are needed to ensure safety, quality and efficacy of these herbal medicines. SeptilinTM, a proprietary herbal medicinal product has been reported to have immunomodulatory effects. Methods: For this narrative review the author surveyed the primary literature on SeptilinTM and its ingredients with regards to immunomodulatory, nitric oxide (NO) and cytokine activity. Databases utilized included Pubmed, Science Direct and EBSCO, Google Scholar as well as a hand search through journals and bibliographies was included. English language restriction was observed. The following parameters had to be met for study inclusion: investigations on SeptilinTM as a formulation (liquid or dried form) were accepted. Research on the isolated constituents of SeptilinTM (single herbs) was also accepted. The accepted model types included; in vitro and in vivo, animal and human models. The following were also required; method of preparation of the SeptilinTM, concentration of the plant preparation and dose/exposure time. Only studies providing statistically significant results with regards to immunomodulatory, cytokine and nitric oxide activity were included. Results: SeptilinTM and its ingredients had effects on at least one cytokine. The most frequently studied cytokines were IL-1, IL-2, IL-4, IL-6, TNF, and IFN. Many studies also reported on NO activities. SeptilinTM and its ingredients demonstrated modulation of several cytokines with varying results on NO activity. The bulk of studies conducted on SeptilinTM and its ingredients were in vitro, the few in vivo studies were mainly conducted in rats or mice models with a few studies conducted on humans. Conclusion: The in vitro and in vivo research demonstrates that SeptilinTM and its ingredients modulate the secretion of multiple cytokines and NO with varying effects on cytokine and NO secretion due to divergent research methodologies. The reported therapeutic success of these herbal products by natural medicine practitioners and clinicians may be due to their effects on cytokine and NO activity. Bangladesh Journal of Medical Science Vol.18(4) 2019 p.675-688

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