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1
Smiljic, Sonja, Vojkan Nestorovic, and Sladjana Savic. "Modulatory role of nitric oxide in cardiac performance." Medical review 67, no. 9-10 (2014): 345–52. http://dx.doi.org/10.2298/mpns1410345s.
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Nitric oxide is produced by almost all cardiac cells, endothelial cells, cardiomyocytes and nerve fibers. It is synthesized by an enzyme, a nitric oxide synthase, which occurs in endothelial, neural and inducible form. The distribution of nitric oxide synthase in the heart is characterized by a pronounced non-uniformity. Nitric oxide exerts its effects in physiological and pathophysiological conditions. The physiological effects of low concentrations of nitric oxide, which is released in the normal conditions under the influence of constituent enzymes, occur via cyclic guanosine monophosphate. The synthesized nitric oxide exhibits its effect in the cells where it is produced, in an autocrine manner, or by diffusing into the neighboring cells, in a paracrine manner. Nitric oxide acts by regulating the coronary vessel tonus, affecting the contractility of cardiomyocytes, generating an inotropic effect in a dose-dependent manner and controlling the cellular respiration. Other effects of nitric oxide in the cardiovascular system include the hyperpolarization of the smooth muscle cells in blood vessels, the inhibition of the monocyte adhesion, the inhibition of platelet migration, adhesion and aggregation and the proliferation of smooth muscle cells and fibroblasts. The anti-atherosclerotic effects of nitric oxide are based on these effects. Nitric oxide is a weak free radical in gaseous state, and the cytotoxic and/or the cytoprotective effects of the higher concentrations of nitric oxide are related to the chemical structure of nitric oxide as a free radical. The excessive production of nitric oxide by the activation of inducible nitric oxide synthase can lead to major irregularities in the function of cardiomyocytes and cardiac insufficiency. Understanding the nitric oxide molecular mechanisms of signaling pathways in the heart can provide a new strategic approach to prevention and treatment of cardiovascular diseases.
2
Ukeri, John, Michael T. Wilson, and Brandon J. Reeder. "Modulating Nitric Oxide Dioxygenase and Nitrite Reductase of Cytoglobin through Point Mutations." Antioxidants 11, no. 9 (September 15, 2022): 1816. http://dx.doi.org/10.3390/antiox11091816.
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Cytoglobin is a hexacoordinate hemoglobin with physiological roles that are not clearly understood. Previously proposed physiological functions include nitric oxide regulation, oxygen sensing, or/and protection against oxidative stress under hypoxic/ischemic conditions. Like many globins, cytoglobin rapidly consumes nitric oxide under normoxic conditions. Under hypoxia, cytoglobin generates nitric oxide, which is strongly modulated by the oxidation state of the cysteines. This gives a plausible role for this biochemistry in controlling nitric oxide homeostasis. Mutations to control specific properties of hemoglobin and myoglobin, including nitric oxide binding/scavenging and the nitrite reductase activity of various globins, have been reported. We have mapped these key mutations onto cytoglobin, which represents the E7 distal ligand, B2/E9 disulfide, and B10 heme pocket residues, and examined the nitric oxide binding, nitric oxide dioxygenase activity, and nitrite reductase activity. The Leu46Trp mutation decreases the nitric oxide dioxygenase activity > 10,000-fold over wild type, an effect 1000 times greater than similar mutations with other globins. By understanding how particular mutations can affect specific reactivities, these mutations may be used to target specific cytoglobin activities in cell or animal models to help understand the precise role(s) of cytoglobin under physiological and pathophysiological conditions.
3
Sibgatullin, I. T., R. Ya Gilmutdinov, and T. M. Zakirov. "The Effect of the Drug Estrofan on the Content of Nitric Oxide (II), Sex Hormones, Biochemical Parameters and Their Relationship in Cows." BIO Web of Conferences 37 (2021): 00170. http://dx.doi.org/10.1051/bioconf/20213700170.
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The physiological functions of nitric oxide (II) are diverse, and its therapeutic uses continue to expand. Many methods have been found to regulate the production of this compound, both physiological, regulated by the body itself, and as a result of various, drug and non-drug, external influences, correcting the ability of cells, organs and tissues to produce nitric oxide (II). The drug estrophan (synthetic prostaglandin PGF2α) has an activating effect on the nitric oxide (II) system and on sex hormones that regulate the reproductive functions of cows. The introduction of estrophan to cows is accompanied by an increase in the synthesis of nitric oxide (II), estrogen in the body of cows, and a decrease in progesterone. A high level of interrelation of estrogen with nitric oxide (II) was shown, the value of the correlation coefficient is (r = 0.552; p < 0.05). Correlation of the level of nitric oxide (II) with estrogen allows making an assumption of its bioregulatory functions, including the sexual cycle. The introduction of estrophan had no effect on the biochemical parameters in the blood serum of cows.
4
Jovic, Slavoljub, Jelka Stevanovic, Suncica Borozan, Blagoje Dimitrijevic, Svetlana Fister, and Jelena Aleksic. "Useful and harmful effects of nitric oxide." Veterinarski glasnik 67, no. 3-4 (2013): 245–57. http://dx.doi.org/10.2298/vetgl1304245j.
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In living sistems synthesis of nitric oxide occurs during metabolism from Larginin, nitrite and ascorbate. Being very significant carrier of information within numerous both physiological and pathological proceses in mammals' organisms, nitric oxid could possibly be useful as well as harmful. Nitric oxide synthesis is adjuvant in a healthy organism because it represents the basic molecule for understanding numerous processes in neurology, psychology, immunology and varios related fields. In other words, nitric oxide participate in number of physiological processes, such as: transmission of nerve signals (neurotransmitter role), regulation of smooth muscle tissue relaxation (eg. vasodilatation), peristaltic movements, immunomodulation, mastocyte activation, development of inflammatory response, apoptosis regulation, angiogenesis and glucose metabolism, normal heart functioning and antioxidation role. Besides being useful, nitric oxide can be harmful as well, because it has one unpaired electron, so consequently it is susceptible to oxidation becoming a stable free radical. Being such, it reacts quickly with superoxide-anion radical, givind at first an extremely reactive peroxinitrite anion, and subsequently peroxidnitrite acid. This acid is very dangerous causing thiol groups oxidation, tyrosine and phenylalanine nitrosylation, lipid oxidation, DNK chain splitting, nitrification and nucleic bases deamination. These damages of macromolecules can cause a series of undesirable changes which subsequently distub functions of molecules, and thus of cells, tissues and even organs.
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Muftin, Najlaa Qassim, Asma Jameil Al-Lamei, Suzanne Jubair, Abdalla Raied Jabber, and Rasha Shakir Mahmood. "The Role Of Nitric Oxide In Cancer Development & it`s Therapy." Journal of advanced Sciences and Engineering Technologies 3, no. 1 (January 3, 2020): 21–34. http://dx.doi.org/10.32441/jaset.03.01.02.
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The Nitric oxide is a free radical belongs to reactive nitrogen species, acts as a signal molecule in many physiological and pathological processes as well as plays a significant role in a variety of biological processes including its action as a regulator to programmed cell death (apoptosis). In addition to its role in tumor formation, proliferation, and metastasis, Nitric oxide has also been stated to have tumoricidal effects. Therefore this review deals with the effect of nitric oxide on different types of cancer and its use in cancer drugs
6
Suschek, Christoph V., Dennis Feibel, Maria von Kohout, and Christian Opländer. "Enhancement of Nitric Oxide Bioavailability by Modulation of Cutaneous Nitric Oxide Stores." Biomedicines 10, no. 9 (August 29, 2022): 2124. http://dx.doi.org/10.3390/biomedicines10092124.
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The generation of nitric oxide (NO) in the skin plays a critical role in wound healing and the response to several stimuli, such as UV exposure, heat, infection, and inflammation. Furthermore, in the human body, NO is involved in vascular homeostasis and the regulation of blood pressure. Physiologically, a family of enzymes termed nitric oxide synthases (NOS) generates NO. In addition, there are many methods of non-enzymatic/NOS-independent NO generation, e.g., the reduction of NO derivates (NODs) such as nitrite, nitrate, and nitrosylated proteins under certain conditions. The skin is the largest and heaviest human organ and contains a comparatively high concentration of these NODs; therefore, it represents a promising target for many therapeutic strategies for NO-dependent pathological conditions. In this review, we give an overview of how the cutaneous NOD stores can be targeted and modulated, leading to a further accumulation of NO-related compounds and/or the local and systemic release of bioactive NO, and eventually, NO-related physiological effects with a potential therapeutical use for diseases such as hypertension, disturbed microcirculation, impaired wound healing, and skin infections.
7
Suresh, Vinod, David A. Shelley, Hye-Won Shin, and Steven C. George. "Effect of heterogeneous ventilation and nitric oxide production on exhaled nitric oxide profiles." Journal of Applied Physiology 104, no. 6 (June 2008): 1743–52. http://dx.doi.org/10.1152/japplphysiol.01355.2007.
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Elevated exhaled nitric oxide (NO) in the breath of asthmatic subjects is thought to be a noninvasive marker of lung inflammation. Asthma is also characterized by heterogeneous bronchoconstriction and inflammation, which impact the spatial distribution of ventilation in the lungs. Since exhaled NO arises from both airway and alveolar regions, and its level in exhaled breath depends strongly on flow, spatial heterogeneity in flow patterns and NO production may significantly affect the exhaled NO signal. To investigate the effect of these factors on exhaled NO profiles, we developed a multicompartment mathematical model of NO exchange using a trumpet-shaped central airway segment that bifurcates into two similarly shaped peripheral airway segments, each of which empties into an alveolar compartment. Heterogeneity in flow alone has only a minimal impact on the exhaled NO profile. In contrast, placing 70% of the total airway NO production in the central compartment or the distal poorly ventilated compartment can significantly increase (35%) or decrease (−10%) the plateau concentration, respectively. Reduced ventilation of the peripheral and acinar regions of the lungs with concomitant elevated NO production delays the rise of NO during exhalation, resulting in a positive phase III slope and reduced plateau concentration (−11%). These features compare favorably with experimentally observed profiles in exercise-induced asthma and cannot be simulated with single-path models. We conclude that variability in ventilation and NO production in asthmatic subjects impacts the shape of the exhaled NO profile and thus impacts the physiological interpretation.
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Cui, X. M., Y. K. Zhang, X. B. Wu, and C. S. Liu. "The investigation of the alleviated effect of copper toxicity by exogenous nitric oxide in tomato plants." Plant, Soil and Environment 56, No. 6 (June 3, 2010): 274–81. http://dx.doi.org/10.17221/98/2009-pse.
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As a bioactive signal, nitric oxide (NO) is involved in multiple plant physiological responses, especially under some abiotic stress. Here, we investigated the effects of exogenous nitric oxide on both the reactive oxygen species (ROS) scavenging metabolism and regulating functions of plasma membrane and tonoplast in tomato plants treated with 50µM CuCl<sub>2</sub>. Copper stress induced significant accumulation of H<sub>2</sub>O<sub>2</sub>, led to serious lipid peroxidation, and finally markedly decreased shoot height and fresh weight of tomato plants. The application of 100µM sodium nitroprusside (SNP – NO donor) promoted some antioxidant enzymes, reduced accumulation of H<sub>2</sub>O<sub>2</sub>, and adjusted the activity of H<sup>+</sup>-ATPase and H<sup>+</sup>-PPase in plasma membrane or tonoplast, and significantly alleviated the growth inhibition induced by copper toxicity. On the other hand, the application of sodium ferrocyanide (an analog of SNP) and sodium nitrate or nitrite (the decomposition product of NO or its donor SNP) which did not release NO, did not show the effects of SNP. Furthermore, the effects of SNP were reverted by addition of hemoglobin (an NO scavenger). Therefore, these results indicated that exogenous NO could effectively assuage copper toxicity by physiological and biochemical response so as to maintain normal growth.
9
Nenasheva, N. M., and N. M. Nenasheva. "ROLE OF NITRIC OXIDE IN EXHALED AIR IN BRONCHIALASTHMA." Russian Journal of Allergy 7, no. 1 (March 15, 2010): 26–31. http://dx.doi.org/10.36691/rja871.
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In this review the main physiological effects of nitric oxide in the human body have been considered, as well as its pathophysiologic role in bronchial asthma. Methods for determination of nitric oxide in exhaled air have been described. The importance of determining the level of nitric oxide in patients with bronchial asthma has been analyzed.
10
Satoh, Nobuhiko, Motonobu Nakamura, Atsushi Suzuki, Hiroyuki Tsukada, Shoko Horita, Masashi Suzuki, Kyoji Moriya, and George Seki. "Effects of Nitric Oxide on Renal Proximal Tubular Na+Transport." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/6871081.
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Nitric oxide (NO) has a wide variety of physiological functions in the kidney. Besides the regulatory effects in intrarenal haemodynamics and glomerular microcirculation,in vivostudies reported the diuretic and natriuretic effects of NO. However, opposite results showing the stimulatory effect of NO on Na+reabsorption in the proximal tubule led to an intense debate on its physiological roles. Animal studies have showed the biphasic effect of angiotensin II (Ang II) and the overall inhibitory effect of NO on the activity of proximal tubular Na+transporters, the apical Na+/H+exchanger isoform 3, basolateral Na+/K+ATPase, and the Na+/HCO3-cotransporter. However, whether these effects could be reproduced in humans remained unclear. Notably, our recent functional analysis of isolated proximal tubules demonstrated that Ang II dose-dependently stimulated human proximal tubular Na+transport through the NO/guanosine 3′,5′-cyclic monophosphate (cGMP) pathway, confirming the human-specific regulation of proximal tubular transport via NO and Ang II. Of particular importance for this newly identified pathway is its possibility of being a human-specific therapeutic target for hypertension. In this review, we focus on NO-mediated regulation of proximal tubular Na+transport, with emphasis on the interaction with individual Na+transporters and the crosstalk with Ang II signalling.
11
Kharitonov, Sergei A., Gert Lubec, Barbara Lubec, Magnus Hjelm, and Peter J. Barnes. "l-Arginine Increases Exhaled Nitric Oxide in Normal Human Subjects." Clinical Science 88, no. 2 (February 1, 1995): 135–39. http://dx.doi.org/10.1042/cs0880135.
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1. Endogenous nitric oxide plays an important physiological role and is synthesized by several isoforms of nitric oxide synthase from the semiessential amino acid l-arginine. Nitric oxide is detectable in the exhaled air of normal individuals and may be used to monitor the formation of nitric oxide in the respiratory tract. 2. We have investigated the effect of orally administered l-arginine (0.05, 0.1, 0.2 g/kg) compared with matched placebo on the concentration of nitric oxide in the exhaled air in 23 normal individuals. 3. l-Arginine caused significant increases in the concentration of nitric oxide in exhaled air at doses of 0.1 and 0.2 mg/kg, which was maximal 2 h after administration. This was associated with an increase in the concentration of l-arginine and nitrate in plasma. There were no significant changes in heart rate, blood pressure or forced expiratory volume in 1 s. 4. These results suggest that an increase in the amount of substrate for nitric oxide synthase can increase the formation of endogenous nitric oxide. This may have therapeutic relevance in diseases in which there is defective production of nitric oxide.
12
Bautista, A. P., and J. J. Spitzer. "Inhibition of nitric oxide formation in vivo enhances superoxide release by the perfused liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 5 (May 1, 1994): G783—G788. http://dx.doi.org/10.1152/ajpgi.1994.266.5.g783.
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Nitric oxide, a known scavenger of toxic oxygen-derived radicals, has been shown to have a protective effect against tissue injury in endotoxemia. Based on the hypothesis that under normal physiological conditions, a balance between superoxide and nitric oxide exists in vivo, this work examines hepatic superoxide release after nitric oxide formation is inhibited in vivo. Male Sprague-Dawley rats were treated intravenously with N omega-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg body wt), an inhibitor of nitric oxide synthase. One hour later, superoxide anion release by the perfused liver was determined. Results show that a significant amount of superoxide was released after L-NAME treatment. Likely sources of this radical are the Kupffer cells. Inhibition of nitric oxide formation in vivo did not enhance superoxide release by hepatocytes or sinusoidal endothelial cells. The effect of L-NAME treatment on superoxide release in endotoxemic rats was also examined 12 h after lipopolysaccharide treatment, when toxic oxygen-derived radical formation could not be detected. Inhibition of nitric oxide release in vivo in these rats enhanced the formation of superoxide anion. The interaction between nitric oxide and superoxide anion under normal conditions may represent an important protective mechanism of the host against free radical damage.
13
Okudaira, Mariko, Yasuo Ontachi, Tomoe Mizutani, Mika Omote, Tomotaka Yoshida, Minori Kaneda, Masahide Yamazaki, et al. "Antithrombotic role of nitric oxide in rats under physiological conditions." Thrombosis and Haemostasis 91, no. 01 (2004): 71–75. http://dx.doi.org/10.1160/th03-05-0292.
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SummaryAlthough sepsis-induced release of nitric oxide (NO) is known to have an antithrombotic effect, it is unknown if NO exerts this same effect under physiological conditions. We have therefore attempted to determine whether or not NO protects against thrombus formation in normal Wistar rats injected with various amounts (0.8, 4.0, 20.0 and 100mg/kg/4hr) of L-NAME (N (omega)-nitro-l-arginine methyl ester), an NO synthase inhibitor, via the tail vein. Plasma levels of D-dimer fragments of fibrin were significantly increased in rats receiving L-NAME (0.21±0.04, 0.22±0.05, 0.26±0.07, 0.59±0.17µg/mL, means±SE; p<0.05, 0.05, 0.05, 0.01: L-NAME 0.8, 4, 20, 100, respectively, compared with control levels: <0.06 µg/mL), and thrombin-antithrombin complex (TAT) levels were significantly increased in rats receiving 20mg/kg/4hr or greater doses of L-NAME (4.5±1.1, 4.7±1.4, 18.7±4.9, 42.5±4.0ng/mL, NS, NS, p<0.05, 0.01, respectively, compared with control levels: 3.8±1.2 ng/mL). Glomerular fibrin deposition was increased in a dose-dependent manner in rats receiving L-NAME (6.8±1.5, 13.9±1.6, 32.4±2.6, 49.2±5.2%, p<0.05, 0.05, 0.01, 0.01, respectively, compared with control levels: 0.0±0.0%). Renal dysfunction and hepatic dysfunction were observed in rats receiving 20mg/kg/4hr or greater, or 100mg/kg/4hr, doses of L-NAME, respectively. Mean blood pressure was also elevated in rats receiving L-NAME in a dose-dependent manner. These findings suggest that NO, in addition to regulating blood pressure, is involved in prevention of thrombus formation under physiological circumstances.
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Reid, MB. "Reactive Oxygen and Nitric Oxide in Skeletal Muscle." Physiology 11, no. 3 (June 1, 1996): 114–19. http://dx.doi.org/10.1152/physiologyonline.1996.11.3.114.
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Skeletal muscle produces oxygen radicals, nitric oxide, and a variety of redox-active derivatives that modulate muscle function under physiological conditions. In unfatigued muscle, reactive oxygen intermediates and nitric oxide exert opposing effects on excitation-contraction coupling. During strenuous exercise, oxidants accumulate in the tissue and accelerate the fatigue process.
15
Lefer, Allan M., and David J. Lefer. "II. Nitric oxide protects in intestinal inflammation." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (March 1, 1999): G572—G575. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g572.
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This article examines the evidence for nitric oxide (NO) as a protective agent in splanchnic ischemia-reperfusion and other forms of acute intestinal inflammation. Four major points emerge from this body of data. First, acute intestinal inflammation results in an early (i.e., <5 min) and severe decrease in endothelium-derived NO. Thus the early trigger event in this condition is a functional loss of NO. Second, administration of exogenous NO, NO donors, or NO precursors ameliorate splanchnic ischemia-reperfusion and other forms of acute intestinal inflammation (i.e., splanchnic trauma). These beneficial effects occur at physiological levels of NO when given early in the course of the inflammatory state. Third, blockade of nitric oxide synthase (NOS) or gene deletion of NOS exacerbates intestinal inflammation. Fourth, there are a variety of signaling mechanisms that may mediate the protective effect of NO.
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Murad, Ferid. "Discovery of Some of the Biological Effects of Nitric Oxide and its Role in Cell Signaling." Bioscience Reports 19, no. 3 (June 1, 1999): 133–54. http://dx.doi.org/10.1023/a:1020265417394.
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The role of nitric oxide in cellular signaling in the past 22 years has become one of the most rapidly growing areas in biology with more than 20,000 publications to date. Nitric oxide is a gas and free radical with an unshared electron that can regulate an ever-growing list of biological processes. In many instances nitric oxide mediates its biological effects by activating guanylyl cyclase and increasing cyclic GMP synthesis from GTP. However, the list of effects of nitric oxide that are independent of cyclic GMP is also growing at a rapid rate. For example, nitric oxide can interact with transition metals such as iron, thiol groups, other free radicals, oxygen, superoxide anion, unsaturated fatty acids and other molecules. Some of these reactions result in the oxidation of nitric oxide to nitrite and nitrate to terminate its effect, while other reactions can lead to altered protein structure, function, and/or catalytic capacity. These diverse effects of nitric oxide that are either cyclic GMP dependent or independent can alter and regulate important physiological and biochemical events in cell regulation and function. Nitric oxide can function as an intracellular messenger, an autacoid, a paracrine substance, a neurotransmitter, or as a hormone that can be carried to distant sites for effects. Thus, it is a unique simple molecule with an array of signaling functions. However, as with any messenger molecule, there can be too little or too much of the substance and pathological events result. Some of the methods to regulate either nitric oxide formation, metabolism, or function have been in clinical use for more than a century as with the use of organic nitrates and nitroglycerin in angina pectoris that was initiated in the 1870's. Current and future research with nitric oxide and cyclic GMP will undoubtedly expand the clinicians' therapeutic armamentarium to manage a number of important diseases by perturbing nitric oxide and cyclic GMP formation and metabolism. Such promise and expectations have obviously fueled the interests in these signaling molecules for a growing list of potential therapeutic applications.
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Murad, Ferid. "Discovery of Some of the Biological Effects of Nitric Oxide and its Role in Cell Signaling." Bioscience Reports 24, no. 4-5 (August 10, 2004): 452–74. http://dx.doi.org/10.1007/s10540-005-2741-8.
Full textAbstract:
The role of nitric oxide in cellular signaling in the past 22 years has become one of the most rapidly growing areas in biology with more than 20,000 publications to date. Nitric oxide is a gas and free radical with an unshared electron that can regulate an ever-growing list of biological processes. In many instances nitric oxide mediates its biological effects by activating guanylyl cyclase and increasing cyclic GMP synthesis from GTP. However, the list of effects of nitric oxide that are independent of cyclic GMP is also growing at a rapid rate. For example, nitric oxide can interact with transition metals such as iron, thiol groups, other free radicals, oxygen, superoxide anion, unsaturated fatty acids and other molecules. Some of these reactions result in the oxidation of nitric oxide to nitrite and nitrate to terminate its effect, while other reactions can lead to altered protein structure, function, and/or catalytic capacity. These diverse effects of nitric oxide that are either cyclic GMP dependent or independent can alter and regulate important physiological and biochemical events in cell regulation and function. Nitric oxide can function as an intracellular messenger, an autacoid, a paracrine substance, a neurotransmitter, or as a hormone that can be carried to distant sites for effects. Thus, it is a unique simple molecule with an array of signaling functions. However, as with any messenger molecule, there can be too little or too much of the substance and pathological events result. Some of the methods to regulate either nitric oxide formation, metabolism, or function have been in clinical use for more than a century as with the use of organic nitrates and nitroglycerin in angina pectoris that was initiated in the 1870's. Current and future research with nitric oxide and cyclic GMP will undoubtedly expand the clinicians' therapeutic armamentarium to manage a number of important diseases by perturbing nitric oxide and cyclic GMP formation and metabolism. Such promise and expectations have obviously fueled the interests in these signaling molecules for a growing list of potential therapeutic applications.
18
Romero, J. C., V. Lahera, M. G. Salom, and M. L. Biondi. "Role of the endothelium-dependent relaxing factor nitric oxide on renal function." Journal of the American Society of Nephrology 2, no. 9 (March 1992): 1371–87. http://dx.doi.org/10.1681/asn.v291371.
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The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.
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Karthikesh, Madhumithra Subramanian, and Xinmai Yang. "The effect of ultrasound cavitation on endothelial cells." Experimental Biology and Medicine 246, no. 7 (January 18, 2021): 758–70. http://dx.doi.org/10.1177/1535370220982301.
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Acoustic cavitation has been widely explored for both diagnostic and therapeutic purposes. Ultrasound-induced cavitation, including inertial cavitation and non-inertial cavitation, can cause microstreaming, microjet, and free radical formation. The acoustic cavitation effects on endothelial cells have been studied for drug delivery, gene therapy, and cancer therapy. Studies have demonstrated that the ultrasound-induced cavitation effect can treat cancer, ischaemia, diabetes, and cardiovascular diseases. In this minireview, we will review the impact of ultrasound-induced cavitation on the endothelial cells such as cell permeability, cell proliferation, gene expression regulation, cell viability, hemostasis interaction, oxygenation, and variation in the level of calcium ions, ceramide, nitric oxide (NO) and nitric oxide synthase (NOS) activity. The applications of these effects and the cavitation mechanism involved will be summarized, demonstrating the important role of acoustic cavitation in non-invasive ultrasound treatment of various physiological conditions.
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Garthwaite, John. "Nitric oxide as a multimodal brain transmitter." Brain and Neuroscience Advances 2 (January 2018): 239821281881068. http://dx.doi.org/10.1177/2398212818810683.
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One of the simplest molecules in existence, nitric oxide, burst into all areas of biology some 30 years ago when it was established as a major signalling molecule in the cardiovascular, nervous and immune systems. Most regions of the mammalian brain synthesise nitric oxide and it has many diverse roles both during development and in adulthood. Frequently, nitric oxide synthesis is coupled to the activation of NMDA receptors and its physiological effects are mediated by enzyme-linked receptors that generate cGMP. Generally, nitric oxide appears to operate in two main modes: first, in a near synapse-specific manner acting either retrogradely or anterogradely and, second, when multiple nearby sources are active simultaneously, as a volume transmitter enabling signalling to diverse targets irrespective of anatomical connectivity. The rapid diffusibility of nitric oxide and the efficient capture of fleeting, subnanomolar nitric oxide concentrations by its specialised receptors underlie these modes of operation.
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Kamosinska, B., M. W. Radomski, M. Duszyk, A. Radomski, and S. F. Man. "Nitric oxide activates chloride currents in human lung epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (June 1, 1997): L1098—L1104. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1098.
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Epithelial Cl- channels are regulated by various physiological factors, including guanosine 3',5'-cyclic monophosphate (cGMP). Because cGMP mediates many of the physiological actions of nitric oxide (NO), we have studied both the presence of endogenous NO and the effects of exogenous NO on Cl- currents in A549 human lung epithelial cells. We have detected Ca(2+)-dependent NO synthase activity in A549 cells. Using the perforated patch-clamp technique, we have shown that inhibition of this enzyme by NG-monomethyl-L-arginine decreased Cl- current, an effect that was reversed by the NO donor S-nitrosoglutathione (GSNO). In addition, the NO donors GSNO and S-nitroso-N-acetyl-D,L-penicillamine increased whole-cell Cl- currents in A549 cells. This stimulatory effect of the NO donors was sensitive to inhibition by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, suggesting that channels other than the cystic fibrosis transmembrane conductance regulator (CFTR) are involved in the action of NO on A549 cells. In addition, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a selective inhibitor of soluble guanylyl cyclase, decreased NO-mediated stimulation of Cl- currents. Our results suggest that, in lung epithelial cells, NO regulates a non-CFTR Cl- conductance acting via a cGMP-dependent mechanism.
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Akanji, Musbau A., Anne A. Adeyanju, Damilare Rotimi, and Oluyomi S. Adeyemi. "Nitric Oxide Balance in Health and Diseases: Implications for New Treatment Strategies." Open Biochemistry Journal 14, no. 1 (July 31, 2020): 25–32. http://dx.doi.org/10.2174/1874091x02014010025.
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Nitric Oxide (NO) is an essential signaling molecule with diverse physiological functions in humans. The steady-state concentration and site of production of nitric oxide determine its effects in biological systems. The human cells are exposed to both beneficial and harmful effects of NO. These dual effects of NO could depend on its local concentration in the cells. Additionally, the rate of synthesis, translocation, direct interaction with other molecules, and signals contribute to the biochemical and physiological effects of NO. In this review, the biochemical and physiological role of NO, particularly in health and disease as touching on cell signaling, oxidative stress, immunity, as well as cardiovascular protection amongst others, is focused on. Therefore, this review objectively discusses the dual functionality of NO in living cells.
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French, Stephanie, Cecilia Giulivi, and R. S. Balaban. "Nitric oxide synthase in porcine heart mitochondria: evidence for low physiological activity." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 6 (June 1, 2001): H2863—H2867. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2863.
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The capacity of isolated porcine heart mitochondria to produce nitric oxide (NO) via mitochondrial NO synthase (NOS) was evaluated. The mitochondrial NOS content and activity (0.2 nmol NO · mg mitochondrial protein−1 · min−1) were ∼10 times lower than previously reported for the rat liver. No evidence for mitochondrial NOS-generated NO was found in mitochondrial suspensions based on the lack of NO production and the lack of effect of eitherl-arginine or NOS inhibitors on the rate of respiration. The reason that even the low mitochondrial NOS activity did not result in net NO production and metabolic effects is because the mitochondrial metabolic breakdown of NO (1–4 nmol NO · mg mitochondrial protein−1 · min−1) was greater than the maximum rate of NO production measured in homogenates. These data suggest that NO production at the mitochondria via NOS is not a significant source of NO in the intact heart and does not regulate cardiac oxidative phosphorylation.
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Borikov, Oleksii, Nataliia Gorbenko, Olha Ivanova, K. V. Taran, T. S. Litvinova, and Tetiana Kiprich. "SEX DIFFERENCES OF ENDOTHELIAL DYSFUNCTION MARKERS — NITRIC OXIDE SYNTHASE AND HEME OXYGENASE IN RATS WITH 2 TYPE DIABETES MELLITUS." Problems of Endocrine Pathology 66, no. 4 (December 3, 2018): 37–43. http://dx.doi.org/10.21856/j-pep.2018.4.04.
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The effect of type 2 diabetes on the markers of endothelial dysfunction — nitric oxide synthase and heme oxygenase has been studied in rats, depending on sex. It was established that the activity of nitric oxide synthase in the blood vessels of female rats is significantly higher in comparison with males under physiological conditions. Type 2 diabetes leads to the different depression of the nitric oxide synthase activity in the blood vessels of females and males, which eliminates sexual differences in the activity of this enzyme. It was found that in contrast to nitric oxide synthase, the activity of heme oxygenase in vascular homogenate does not depend on the sex of intact animals. Type 2 diabetes leads to more expressive increase in heme oxygenase activity in female blood vessels compared to male rats. We can suppose that a more pronounced elevation of the heme oxygenase activity in case of a decrease the nitric oxide synthase activity is a compensatory mechanism for reducing of endothelial dysfunction in women with type 2 diabetes.
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Sibmooh, Nathawut, Barbora Piknova, and Alan N. Schechter. "Ascorbic Acid Catalyzes Nitric Oxide Production from Nitrite Ions." Blood 108, no. 11 (November 16, 2006): 1574. http://dx.doi.org/10.1182/blood.v108.11.1574.1574.
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Abstract We have previously shown that nitrite ions can be reduced by hemoglobin to nitric oxide (NO), a ubiquitous signaling molecule and potent vasodilator. Nitrite serves as a stable tissue and vascular source for NO production; the reduction reaction is maximal at about 50% oxygen saturation values and is enhanced at low pH but little is known about other effectors of this reaction. In the current work, we studied the effect of ascorbic acid on nitrite reduction under physiological conditions using chemiluminescence to quantify NO production. In physiological buffer, this reaction has a rate constant of about 1×10−5 M−1.s−1. Thus, a significant production of NO would likely occur in plasma only at pharmacological levels of ascorbic acid (> 1 mM) although lowering pH below 7.0 markedly enhances this reaction. Loading human erythrocytes with 0.5 mM dehydroascorbic acid, which is in redox equilibrium with ascorbic acid and which can significantly raise intracellular ascorbic acid levels, increased basal levels of nitrite ions from 42±9.0 nM to 98±56 nM. Uptake of nitrite ions into erythrocytes by incubation in 10 μM nitrite was increased about 1.5 fold by dehydroascorbic acid and the half-time of nitrite loss was slowed to the same extent. Ascorbic acid also reduced free ferric heme in erythrocytes and plasma to ferrous heme which catalyzed the reduction of nitrite to NO with a rate constant of 2.3×103 M−1.s−1 under physiological conditions. However, free ferrous ions did not significantly produce NO in physiological buffer (rate constant = 1.8×10−2 M−1.s−1). The reaction of ferrous heme with nitrite was not affected by heme binding to proteins such as hemopexin and albumin, or erythrocyte membranes. These results suggest that physiological levels of ascorbic acid (20–80 μM in plasma and erythrocytes) may act to catalyze NO production in the blood by promoting the reduction of nitrite ions by free ferrous heme and by increasing intra-erythrocytic levels of nitrite ions which can be reduced to NO by deoxyhemoglobin.
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Mabrouk, Nesrine, Silvia Ghione, Véronique Laurens, Stéphanie Plenchette, Ali Bettaieb, and Catherine Paul. "Senescence and Cancer: Role of Nitric Oxide (NO) in SASP." Cancers 12, no. 5 (May 2, 2020): 1145. http://dx.doi.org/10.3390/cancers12051145.
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Cellular senescence is a cell state involved in both physiological and pathological processes such as age-related diseases and cancer. While the mechanism of senescence is now well known, its role in tumorigenesis still remains very controversial. The positive and negative effects of senescence on tumorigenesis depend largely on the diversity of the senescent phenotypes and, more precisely, on the senescence-associated secretory phenotype (SASP). In this review, we discuss the modulatory effect of nitric oxide (NO) in SASP and the possible benefits of the use of NO donors or iNOS inducers in combination with senotherapy in cancer treatment.
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Becerril, Sara, Amaia Rodríguez, Victoria Catalán, Beatriz Ramírez, Xabier Unamuno, Piero Portincasa, Javier Gómez-Ambrosi, and Gema Frühbeck. "Functional Relationship between Leptin and Nitric Oxide in Metabolism." Nutrients 11, no. 9 (September 6, 2019): 2129. http://dx.doi.org/10.3390/nu11092129.
Full textAbstract:
Leptin, the product of the ob gene, was originally described as a satiety factor, playing a crucial role in the control of body weight. Nevertheless, the wide distribution of leptin receptors in peripheral tissues supports that leptin exerts pleiotropic biological effects, consisting of the modulation of numerous processes including thermogenesis, reproduction, angiogenesis, hematopoiesis, osteogenesis, neuroendocrine, and immune functions as well as arterial pressure control. Nitric oxide (NO) is a free radical synthesized from L-arginine by the action of the NO synthase (NOS) enzyme. Three NOS isoforms have been identified: the neuronal NOS (nNOS) and endothelial NOS (eNOS) constitutive isoforms, and the inducible NOS (iNOS). NO mediates multiple biological effects in a variety of physiological systems such as energy balance, blood pressure, reproduction, immune response, or reproduction. Leptin and NO on their own participate in multiple common physiological processes, with a functional relationship between both factors having been identified. The present review describes the functional relationship between leptin and NO in different physiological processes.
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Cabilla, Jimena P., Sonia A. Ronchetti, Silvana I. Nudler, Eliana A. Miler, Fernanda A. Quinteros, and Beatriz H. Duvilanski. "Nitric oxide sensitive-guanylyl cyclase subunit expression changes during estrous cycle in anterior pituitary glands." American Journal of Physiology-Endocrinology and Metabolism 296, no. 4 (April 2009): E731—E737. http://dx.doi.org/10.1152/ajpendo.90795.2008.
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17β-Estradiol (E2) exerts inhibitory actions on the nitric oxide pathway in rat adult pituitary glands. Previously, we reported that in vivo E2 acute treatment had opposite effects on soluble guanylyl cyclase (sGC) subunits, increasing α1- and decreasing β1-subunit protein and mRNA expression and decreasing sGC activity in immature rats. Here we studied the E2 effect on sGC protein and mRNA expression in anterior pituitary gland from adult female rats to address whether the maturation of the hypothalamus-pituitary axis influences its effects and to corroborate whether these effects occur in physiological conditions such as during estrous cycle. E2 administration causes the same effect on sGC as seen in immature rats, and these effects are estrogen receptor dependent. These results suggest that E2 is the main effector of these changes. Since the sGC α-subunit increases while the sGC activity decreases, we studied if other less active isoforms of the sGC α-subunit are expressed. Here we show for the first time that sGCα2 and sGCα2 inhibitory (α2i) isoforms are expressed in this gland, but only sGCα2i mRNA increased after E2 acute treatment. Finally, to test whether E2 effects take place under a physiological condition, sGC subunit expression was monitored over estrous cycle. sGCα1, -β1, and -α2i fluctuate along estrous cycle, and these changes are directly related with E2 level fluctuations rather than to NO level variations. These findings show that E2 physiologically regulates sGC expression and highlight a novel mechanism by which E2 downregulates sGC activity in rat anterior pituitary gland.
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Amarnani, Saral, Belinda Sangrat, and Gautam Chaudhuri. "Effects of selected endothelium-dependent vasodilators on fetoplacental vasculature: physiological implications." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 2 (August 1, 1999): H842—H847. http://dx.doi.org/10.1152/ajpheart.1999.277.2.h842.
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The endothelium-dependent vasodilators ACh, histamine, and bradykinin were studied in the isolated, perfused human placental cotyledon. Histamine caused a decrease in perfusion pressure that was attenuated by cimetidine. Bradykinin, at lower concentrations (10−20 to 10−14 M), produced a concentration-dependent decrease in perfusion pressure, whereas at higher concentrations it produced an increase in perfusion pressure. ACh was without any effect. The decrease in perfusion pressure observed with bradykinin was potentiated by captopril and was significantly attenuated in the presence of HOE-140, the B2-receptor antagonist, or by pretreatment with an inhibitor of nitric oxide synthase, but not by an inhibitor of cyclooxygenase. The decrease in perfusion pressure observed with bradykinin was potentiated by ANG I but not by ANG II. It is concluded that endothelium-dependent vasodilation can be demonstrated with histamine and bradykinin in the fetoplacental vessels, and at least for bradykinin, this is partly mediated by release of nitric oxide. The potentiation of the bradykinin response in the presence of ANG I may serve to buffer the vasoconstriction produced by ANG II in the fetoplacental circulation.
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Naseem, K. M., and K. R. Bruckdorfer. "Hydrogen peroxide at low concentrations strongly enhances the inhibitory effect of nitric oxide on platelets." Biochemical Journal 310, no. 1 (August 15, 1995): 149–53. http://dx.doi.org/10.1042/bj3100149.
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Simultaneous application of NO and H2O2 to human platelets at physiologically relevant concentrations increased inhibition of platelet aggregation by NO almost 100-fold. If NO and H2O2 were mixed before the addition to platelets, the inhibitory effect remained but still depended on the presence of NO. This suggested an enhanced sensitivity of the platelets to residual NO in the presence of H2O2. The inhibition by the NO/H2O2 mixture was not due to peroxynitrite and was only partly reversed by radical scavengers. The mechanism includes enhanced formation of cyclic GMP in response to NO in the presence of H2O2. H2O2 may play a positive physiological role by amplification and/or prolongation of the action of NO.
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Bradley, Sophie A., and Joern R. Steinert. "Nitric Oxide-Mediated Posttranslational Modifications: Impacts at the Synapse." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/5681036.
Full textAbstract:
Nitric oxide (NO) is an important gasotransmitter molecule that is involved in numerous physiological processes throughout the nervous system. In addition to its involvement in physiological plasticity processes (long-term potentiation, LTP; long-term depression, LTD) which can include NMDAR-mediated calcium-dependent activation of neuronal nitric oxide synthase (nNOS), new insights into physiological and pathological consequences of nitrergic signalling have recently emerged. In addition to the canonical cGMP-mediated signalling, NO is also implicated in numerous pathways involving posttranslational modifications. In this review we discuss the multiple effects of S-nitrosylation and 3-nitrotyrosination on proteins with potential modulation of function but limit the analyses to signalling involved in synaptic transmission and vesicular release. Here, crucial proteins which mediate synaptic transmission can undergo posttranslational modifications with either pre- or postsynaptic origin. During normal brain function, both pathways serve as important cellular signalling cascades that modulate a diverse array of physiological processes, including synaptic plasticity, transcriptional activity, and neuronal survival. In contrast, evidence suggests that aging and disease can induce nitrosative stressviaexcessive NO production. Consequently, uncontrolled S-nitrosylation/3-nitrotyrosination can occur and represent pathological features that contribute to the onset and progression of various neurodegenerative diseases, including Parkinson’s, Alzheimer’s, and Huntington’s.
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Grant, Melissa M., and Daniel Jönsson. "Next Generation Sequencing Discoveries of the Nitrate-Responsive Oral Microbiome and Its Effect on Vascular Responses." Journal of Clinical Medicine 8, no. 8 (July 26, 2019): 1110. http://dx.doi.org/10.3390/jcm8081110.
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Cardiovascular disease is a worldwide human condition which has multiple underlying contributing factors: one of these is long-term increased blood pressure—hypertension. Nitric oxide (NO) is a small nitrogenous radical species that has a number of physiological functions including vasodilation. It can be produced enzymatically through host nitric oxide synthases and by an alternative nitrate–nitrite–NO pathway from ingested inorganic nitrate. It was discovered that this route relies on the ability of the oral microbiota to reduce nitrate to nitrite and NO. Next generation sequencing has been used over the past two decades to gain deeper insight into the microbes involved, their location and the effect of their removal from the oral cavity. This review article presents this research and comments briefly on future directions.
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Ferreira, Leonardo Cesar, and Ana Catarina Cataneo. "Nitric oxide in plants: a brief discussion on this multifunctional molecule." Scientia Agricola 67, no. 2 (April 2010): 236–43. http://dx.doi.org/10.1590/s0103-90162010000200017.
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Several studies were carried out in order to improve the knowledge about the occurrence and activity of nitric oxide (NO) in plants. Thus, this review discusses some aspects related to NO in plants such as chemical properties, synthesis pathways, physiological effects, antioxidant action, signal transduction, interaction with plant hormones and gene expression. In the last years, many advances have been obtained regarding NO synthesis and its physiological effects in plants. However, the molecular mechanisms underlying its effects remain poorly understood. It is signalized that tight interplays among NO, Ca2+, cyclic ADP ribose (cADPR), and protein kinases need to be investigated in details. In addition, it has not yet been possible to identify a plant enzyme displaying a nitric oxide synthase (NOS)-like activity. The elucidation of such aspects represents a challenge to future studies.
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Ortiz, Pablo A., and Jeffrey L. Garvin. "Role of nitric oxide in the regulation of nephron transport." American Journal of Physiology-Renal Physiology 282, no. 5 (May 1, 2002): F777—F784. http://dx.doi.org/10.1152/ajprenal.00334.2001.
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Nitric oxide (NO) plays an important role in various physiological processes in the kidney. In vivo experiments first suggested that the natriuretic and diuretic effects caused by NO may be due to decreased NaCl and fluid absorption by the nephron. In the last 10 years, several reports have directly demonstrated a role for NO in modulating transport in different tubule segments. The effects of NO on proximal tubule transport are still controversial. Both stimulation and inhibition of net fluid and bicarbonate have been reported in this segment, whereas only inhibitory effects of NO have been found in Na/H exchanger and Na/K-ATPase activity. The effects of NO in the thick ascending limb are more homogeneous than in the proximal tubule. In this segment, NO decreases net Cl and bicarbonate absorption. A direct inhibitory effect of NO on the Na-K-2Cl cotransporter and the Na/H exchanger has been reported, while NO was found to stimulate apical K channels in this segment. In the collecting duct, NO inhibits Na absorption and vasopressin-stimulated osmotic water permeability. An inhibitory effect of NO on H-ATPase has also been reported in intercalated cells of the collecting duct. Overall, the reported effects of NO in the different nephron segments mostly agree with the natriuretic and diuretic effects observed in vivo. However, the net effect of NO on transport is still controversial in some segments, and in cases like the distal tubule, it has not been studied.
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Martusevich, Andrew K., Lida K. Kovaleva, Konstantin A. Karuzin, Alexandra V. Surovegina, and Mikhail Yu Artamonov. "Influence of Physiological Donor of Nitric Oxide on Blood Serum Crystallostasis in Rats." Biomedical and Pharmacology Journal 15, no. 1 (March 31, 2022): 499–504. http://dx.doi.org/10.13005/bpj/2390.
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The aim of the work was to study the effect of intraperitoneal administration of dinitrosyl iron complexes with glutathione ligands on the initiated crystallogenesis of rat blood serum. The experiment was performed on 70 male Wistar rats divided into 7 equal groups. The first group of animals was intact (without any manipulation). Rats included in the other groups were administered intraperitoneal injection of 1 ml. 0.9% sodium chloride solution daily for 10 days. At the same time, animals of the third to sixth groups were additionally added to the injected solution with dinitrosyl iron complexes with glutathione ligands (the concentration of the agent was 0.15; 0.30; 0.45 and 0.60 mM, respectively). The rats of the seventh group received 1 ml. an aqueous solution of glutathione (0.15 mM). The study of the effect of DNIC on the crystallogenic properties of rat blood serum was carried out by the method of comparative tezioraphy using a special system of criteria. The data obtained as a result of this study indicate the presence of modification of the crystallogenic (initiating) properties of rat blood serum during the course intraperitoneal administration of a physiological donor of nitric oxide to animals – DNIC, and this effect turns out to be dose-dependent and having an extremum in the region of 0.3-0.45 mM. Taking into account the fact that the crystallogenic properties are a reflection of the component composition and one of the physico-chemical parameters of the biological fluid, it can be assumed that the metabolic response of the body to the use of the compound is also dose-dependent. At the same time, relatively low doses of the agent have the most optimal effect on metabolic processes, stimulating the antioxidant potential of blood serum with a corresponding decrease in the intensity of lipid peroxidation processes, contributing to the optimization of energy metabolism and increasing the activity of detoxification enzyme systems. The results of the teziographic evaluation of animal blood serum samples after a course of injections of DNIC in various concentrations clearly indicate the activating effect of the compound with respect to the crystallogenic (initiating) properties of biological fluid, which is most pronounced when using the substance in 0.3- and 0.45-millimolar aqueous solutions.
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Raoofi, Amir, Ayoob Rostamzadeh, Reza Ahmadi, and Mahdi Heydari. "Effects of nitric oxide on reproductive organs and related physiological processes." Asian Pacific Journal of Reproduction 9, no. 4 (2020): 159. http://dx.doi.org/10.4103/2305-0500.288583.
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Mehta, Bhupesh, Gulnaz Begum, Nanda B. Joshi, and Preeti G. Joshi. "Nitric Oxide–mediated Modulation of Synaptic Activity by Astrocytic P2Y Receptors." Journal of General Physiology 132, no. 3 (August 25, 2008): 339–49. http://dx.doi.org/10.1085/jgp.200810043.
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We investigated the mechanism of synaptic suppression by P2Y receptors in mixed hippocampal cultures wherein networked neurons exhibit synchronized Ca2+ oscillations (SCO) due to spontaneous glutamatergic synaptic transmission. Pharmacological studies suggested that SCO suppression was mediated by P2Y2/P2Y4 receptors. Immunostaining studies and characterization of ATP/UTP-stimulated Ca2+ responses in solitary neurons and astrocytes revealed that the SCO attenuation was effectuated by astrocytes. We demonstrate that nitric oxide released from activated astrocytes causes synaptic suppression by inhibiting neurotransmitter release. Physiological concentrations of ATP and UTP evoked NO production in astrocytes. SCO suppression was considerably diminished by removal of extracellular NO by membrane-impermeable scavenger c-PTIO or by pretreatment of cells with nitric oxide synthase inhibitor L-NAME. The nitric oxide donor DETA/NO effectively suppressed the SCO. ATP/UTP inhibited KCl-induced exocytosis at presynaptic terminals in an NO-dependent manner. In the absence of exogenously added ATP/UTP, both the NO scavenger and NOS inhibitor enhanced the frequency of SCO, implying that astrocytes release NO during spontaneous synaptic activity and exert a suppressive effect. We report for the first time that under physiological conditions astrocytes use NO as a messenger molecule to modulate the synaptic strength in the networked neurons.
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Prado, Carla M., Edna A. Leick-Maldonado, David I. Kasahara, Vera L. Capelozzi, Milton A. Martins, and Iolanda F. L. C. Tibério. "Effects of acute and chronic nitric oxide inhibition in an experimental model of chronic pulmonary allergic inflammation in guinea pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 4 (October 2005): L677—L683. http://dx.doi.org/10.1152/ajplung.00010.2005.
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Endogenously produced nitric oxide is a recognized regulator of physiological lung events, such as a neurotransmitter and a proinflammatory mediator. We tested the differences between chronic and acute nitric oxide inhibition by Nω-nitro-l-arginine methyl ester (l-NAME) treatment in lung mechanics, inflammation, and airway remodeling in an experimental asthma model in guinea pigs. Both acute and chronic l-NAME treatment reduced exhaled nitric oxide in sensitized animals ( P < 0.001). Chronic l-NAME treatment increased baseline and maximal responses after antigen challenge of respiratory system resistance and reduced peribronchial edema and mononuclear cells airway infiltration ( P < 0.05). Acute administration of l-NAME increased maximal values of respiratory system elastance and reduced mononuclear cells and eosinophils in airway wall ( P < 0.05). Chronic ovalbumin exposure resulted in airway wall thickening due to an increase in collagen content ( P < 0.005). Chronic nitric oxide inhibition increased collagen deposition in airway wall in sensitized animals ( P < 0.05). These data support the hypothesis that in this model nitric oxide acts as a bronchodilator, mainly in proximal airways. Furthermore, chronic nitric oxide inhibition was effective in reducing edema and mononuclear cells in airway wall. However, airway eosinophilic inflammation was unaltered by chronic l-NAME treatment. In addition, nitric oxide inhibition upregulates collagen deposition in airway walls.
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Chang, Jason Y. H., W. Daniel Stamer, Jacques Bertrand, A. Thomas Read, Catherine M. Marando, C. Ross Ethier, and Darryl R. Overby. "Role of nitric oxide in murine conventional outflow physiology." American Journal of Physiology-Cell Physiology 309, no. 4 (August 15, 2015): C205—C214. http://dx.doi.org/10.1152/ajpcell.00347.2014.
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Elevated intraocular pressure (IOP) is the main risk factor for glaucoma. Exogenous nitric oxide (NO) decreases IOP by increasing outflow facility, but whether endogenous NO production contributes to the physiological regulation of outflow facility is unclear. Outflow facility was measured by pressure-controlled perfusion in ex vivo eyes from C57BL/6 wild-type (WT) or transgenic mice expressing human endothelial NO synthase (eNOS) fused to green fluorescent protein (GFP) superimposed on the endogenously expressed murine eNOS (eNOS-GFPtg). In WT mice, exogenous NO delivered by 100 μM S-nitroso- N-acetylpenicillamine (SNAP) increased outflow facility by 62 ± 28% (SD) relative to control eyes perfused with the inactive SNAP analog N-acetyl-d-penicillamine (NAP; n = 5, P = 0.016). In contrast, in eyes from eNOS-GFPtg mice, SNAP had no effect on outflow facility relative to NAP (−9 ± 4%, P = 0.40). In WT mice, the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10 μM) decreased outflow facility by 36 ± 13% ( n = 5 each, P = 0.012), but 100 μM l-NAME had no detectable effect on outflow facility (−16 ± 5%, P = 0.22). An eNOS-selective inhibitor (cavtratin, 50 μM) decreased outflow facility by 19 ± 12% in WT ( P = 0.011) and 39 ± 25% in eNOS-GFPtg ( P = 0.014) mice. In the conventional outflow pathway of eNOS-GFPtg mice, eNOS-GFP expression was localized to endothelial cells lining Schlemm's canal and the downstream vessels, with no apparent expression in the trabecular meshwork. These results suggest that endogenous NO production by eNOS within endothelial cells of Schlemm's canal or downstream vessels contributes to the physiological regulation of aqueous humor outflow facility in mice, representing a viable strategy to more successfully lower IOP in glaucoma.
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Asiimwe, Nicholas, Seung Geun Yeo, Min-Sik Kim, Junyang Jung, and Na Young Jeong. "Nitric Oxide: Exploring the Contextual Link with Alzheimer’s Disease." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/7205747.
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Neuronal inflammation is a systematically organized physiological step often triggered to counteract an invading pathogen or to rid the body of damaged and/or dead cellular debris. At the crux of this inflammatory response is the deployment of nonneuronal cells: microglia, astrocytes, and blood-derived macrophages. Glial cells secrete a host of bioactive molecules, which include proinflammatory factors and nitric oxide (NO). From immunomodulation to neuromodulation, NO is a renowned modulator of vast physiological systems. It essentially mediates these physiological effects by interacting with cyclic GMP (cGMP) leading to the regulation of intracellular calcium ions. NO regulates the release of proinflammatory molecules, interacts with ROS leading to the formation of reactive nitrogen species (RNS), and targets vital organelles such as mitochondria, ultimately causing cellular death, a hallmark of many neurodegenerative diseases. AD is an enervating neurodegenerative disorder with an obscure etiology. Because of accumulating experimental data continually highlighting the role of NO in neuroinflammation and AD progression, we explore the most recent data to highlight in detail newly investigated molecular mechanisms in which NO becomes relevant in neuronal inflammation and oxidative stress-associated neurodegeneration in the CNS as well as lay down up-to-date knowledge regarding therapeutic approaches targeting NO.
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Hadi, Faheem, Tahir Maqbool, Tahir Muhammad, Shabana Akhtar, Muhammad Rafiq, Sana Javed Awan, Tania Ahmad Shakoori, and Asima Tayyeb. "A Review on anticancer potential of Nitric Oxide." International Journal of Natural Medicine and Health Sciences 1, no. 4 (September 30, 2022): 31–35. http://dx.doi.org/10.52461/ijnms.v1i4.1018.
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Nitrous oxide (N2O; laughing gas) is clinically used as a safe anesthetic (dentistry, ambulance, childbirth) and is appreciated for its anti-anxiety effect. Nitrous oxide (N2O) is a free radical gas that performs various physiological and pathological processes in the body. NO is produced by different enzymatic pathways and plays a role in homeostasis. Over the past years, NO has emerged as a molecule of interest in many ailments including cancer. But its role in cancer is still controversy. It can display dose-dependent anticancer therapy on the one hand and induce pro-cancer properties on the other hand. But as compared to conventional treatments, NO proved better tumor cell resistance. This review mentions the dichotomous nature of NO that may encourage future research assessing the role of NO in cancer prevention and treatment either as a single agent or in combination with other antineoplastic compounds.
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Korokin, Mikhail, Oleg Gudyrev, Vladimir Gureev, Liliya Korokina, Anna Peresypkina, Tatyana Pokrovskaia, Galina Lazareva, Vladislav Soldatov, Mariya Zatolokina, and Mikhail Pokrovskii. "Studies to Elucidate the Effects of Furostanol Glycosides from Dioscorea deltoidea Cell Culture in a Rat Model of Endothelial Dysfunction." Molecules 25, no. 1 (December 31, 2019): 169. http://dx.doi.org/10.3390/molecules25010169.
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Currently, there is no doubt surrounding a theory that the cardiotropic effects of sex hormones can be due to their direct effect on the cardiovascular system. In recent years, interest in the study of steroid glycosides has increased. We studied the effects of furostanol glycosides (protodioscin and deltozid) from the cell culture of the Dioscorea deltoidea (laboratory code DM-05) on the physiological and biochemical parameters of vascular endothelial function in hypoestrogen-induced endothelial dysfunction after bilateral ovariectomy. It was shown that the use of DM-05 at a dose of 1 mg/kg makes it possible to prevent the development of arterial hypertension (the level of systolic blood pressure (SBP) decreases by 9.7% (p < 0.05) and diastolic blood pressure (DBP) by 8.2%), to achieve a decrease in the coefficient of endothelial dysfunction by 1.75 times against the background of a hypoestrogenic state. With DM-05, an increase in the concentration of stable nitric oxide metabolites (NOx) by 45.6% (p < 0.05) and an increase in mRNA endothelial nitric oxide synthase (eNOS) expression by 34.8% (p < 0.05) was established, which indicates a positive effect of furostanol glycosides on the metabolism of nitric oxide after ovariectomy. Positive dynamics in the histological structure of the heart and the abdominal aorta indicate the pronounced endothelio- and atheroprotective effects of DM-05.
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Thomas, Jeffrey E. "Molecular biological considerations in cerebral vasospasm following aneurysmal subarachnoid hemorrhage." Neurosurgical Focus 3, no. 3 (September 1997): E5. http://dx.doi.org/10.3171/foc.1997.3.3.6.
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Chronic delayed cerebral vasospasm (CDCV) remains a serious and often fatal complication of aneurysmal subarachnoid hemorrhage (SAH). The current understanding of its fundamental mechanisms and molecular biological characterization is rudimentary. Two important vasoactive substances have been implicated in CDCV: endothelin-1 (ET-1) and nitric oxide (NO). A 21-amino acid vasoconstrictor peptide, ET-1 has generated interest as a possible important contributor to cerebral vasospasm on the basis of both clinical and experimental evidence suggesting abnormally enhanced production. Nitric oxide is a cell membrane-permeable free radical gas that accounts for the vasodilatory effect of endothelium-derived relaxation factor and is a physiological antagonist of ET-1. As with ET-1, abnormalities of NO production have been implicated in several pathological conditions including cerebral vasospasm. This brief report reviews some of the physiological and regulatory features of these two molecules and explores the possibility of their relationship to cerebral vasospasm.
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Arnal, J. F., J. Yamin, S. Dockery, and D. G. Harrison. "Regulation of endothelial nitric oxide synthase mRNA, protein, and activity during cell growth." American Journal of Physiology-Cell Physiology 267, no. 5 (November 1, 1994): C1381—C1388. http://dx.doi.org/10.1152/ajpcell.1994.267.5.c1381.
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Cell growth influences the expression of several important tissue-specific functions. We sought to examine the effect of cell proliferation on nitric oxide (NO) synthase gene expression in cultured aortic bovine endothelial cells. Western and Northern blot analysis revealed three- and sixfold increases in NO synthase protein and mRNA, respectively, in growing compared with growth-arrested cells. The release of nitrogen oxides was also increased in proliferating cells compared with growth-arrested cells, as was the NO synthase activity assessed by L-arginine/L-citrulline conversion. Neither NO synthase inhibitors nor superoxide dismutase affected proliferation or thymidine incorporation, suggesting that increased NO release had no effect on endothelial cell growth. In conclusion, these studies demonstrate that expression of endothelial cell NO synthase is markedly increased in proliferating compared with quiescent nongrowing cells. The mechanisms underlying this and its physiological consequences remain to be defined.
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Triastuti, Nenny, Muhammad Perdana Airlangga, and Muhammad Anas. "Usage of Inhaled Nitric Oxides in Cases of Eisenmenger Syndrome." Indonesian Journal of Medical Sciences and Public Health 1, no. 1 (June 30, 2020): 13–19. http://dx.doi.org/10.11594/ijmp.01.01.03.
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Eisenmenger Syndrome is congenital heart disease with pulmonary hypertension and shunting turning from right to left. The resistance of pulmonary vascular more than 7.5 mmHg/L/min. The right ventricle and pulmonary artery always enlarge. Physiological effects of inhaled nitric oxide therapy cause selective pulmonary vasodilation: Hypoxia alveoli causes reversible vasoconstriction, thereby increasing pulmonary wedge pressure. Inhaled nitric oxide can lower it. Moderate cardiac output and systematic arterial pressure are not affected; Selective in pulmonary because it is activated by hemoglobin; Selective vasodilation in the ventilated area, local hypoxia alveoli constricts the surrounding vascular tissue and redistributes blood flow to the ventilated lungs better and higher intraalveolar oxygen pressure. Inhaled nitric oxide enhances this mechanism by increasing blood flow through a well-ventilated lung; Bronchodilators; Pulmonary surfactant, The combination of high concentrations of inspired oxygen and high concentrations of Inhaled nitric oxide reduces the minimum surfactant surface tension.
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Balon, Thomas W., and Jerry L. Nadler. "Evidence that nitric oxide increases glucose transport in skeletal muscle." Journal of Applied Physiology 82, no. 1 (January 1, 1997): 359–63. http://dx.doi.org/10.1152/jappl.1997.82.1.359.
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Balon, Thomas W., and Jerry L. Nadler. Evidence that nitric oxide increases glucose transport in skeletal muscle. J. Appl. Physiol. 82(1): 359–363, 1997.—Nitric oxide synthase (NOS) is expressed in skeletal muscle. However, the role of nitric oxide (NO) in glucose transport in this tissue remains unclear. To determine the role of NO in modulating glucose transport, 2-deoxyglucose (2-DG) transport was measured in rat extensor digitorum longus (EDL) muscles that were exposed to either a maximally stimulating concentration of insulin or to an electrical stimulation protocol, in the presence of N G-monomethyl-l-arginine, a NOS inhibitor. In addition, EDL preparations were exposed to sodium nitroprusside (SNP), an NO donor, in the presence of submaximal and maximally stimulating concentrations of insulin. NOS inhibition reduced both basal and exercise-enhanced 2-DG transport but had no effect on insulin-stimulated 2-DG transport. Furthermore, SNP increased 2-DG transport in a dose-responsive manner. The effects of SNP and insulin on 2-DG transport were additive when insulin was present in physiological but not in pharmacological concentrations. Chronic treadmill training increased protein expression of both type I and type III NOS in soleus muscle homogenates. Our results suggest that NO may be a potential mediator of exercise-induced glucose transport.
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BALDRIDGE, WILLIAM H., and ANDY J. FISCHER. "Nitric oxide donor stimulated increase of cyclic GMP in the goldfish retina." Visual Neuroscience 18, no. 6 (November 2001): 849–56. http://dx.doi.org/10.1017/s0952523801186013.
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Nitric oxide (NO) activates soluble guanylyl cyclase (sGC) and the resulting increase in cyclic guanosine monophosphate (cGMP) is an important intracellular signalling pathway in the vertebrate retina. Immunocytochemical detection of cGMP following exposure to NO donors has proven an effective method of identifying cells that express sGC. While such an approach has proven useful for the study of several vertebrate retinas, it has not been applied to the well-characterized teleost retina. Therefore, in the present study, we have applied this approach to the retina of the goldfish (Carassius auratus). In the presence of the phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX), incubation of goldfish eyecups in Ringer's solution containing (±)-S-nitroso-N-acetylpenicillamine (SNAP) increased cGMP-like immunoreactivity (cG-ir) in bipolar, horizontal, amacrine, and ganglion cells and in ganglion cell axons and optic nerve. Weak labeling was observed in horizontal cells but no change in cG-ir was noted within photoreceptors. The NO donor-stimulated increases of cG-ir in horizontal, bipolar, amacrine, and ganglion cells are consistent with known physiological effects of NO on these neurons. The physiological significance of NO action at the level of optic nerve is not known. The lack of an effect of SNAP on cG-ir in photoreceptors was unexpected, as there are known physiological actions of NO, mediated by cGMP, on these neurons. Although this may be due to insufficient sensitivity of immunolabeling, this result may indicate a difference between isoforms of sGC or cGMP PDE in these neurons, compared to neurons where exogenous NO increased cG-ir.
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Zemel, Esther, Orly Eyal, Bo Lei, and Ido Perlman. "NADPH diaphorase activity in mammalian retinas is modulated by the state of visual adaptation." Visual Neuroscience 13, no. 5 (September 1996): 863–71. http://dx.doi.org/10.1017/s0952523800009111.
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AbstractNADPH diaphorase histochemistry is commonly used to identify cells containing nitric oxide synthase (NOS), the enzyme catalyzing the production of nitric oxide from L-arginine. NADPH diaphorase activity and NOS immunostaining was demonstrated in different cells of the vertebrate retina; photoreceptors, horizontal cells, amacrine cells, ganglion cells, and Müller cells. However, the physiological role of nitric oxide (NO) in the retina has yet to be elucidated. In this study, we tested the assumption that NADPH diaphorase activity in the retinas of rabbits and rats depended on the state of visual adaptation. In the rabbit, light adaptation enhanced NADPH diaphorase activity in amacrine cells and practically eliminated it in horizontal cells. Dark adaptation induced the opposite effects; the NADPH diaphorase activity was reduced in amacrine cells and enhanced in horizontal cells. Retinas from eyes that were injected intravitreally with L-glutamate exhibited a pattern of NADPH diaphorase activity that was similar to that seen in dark-adapted retinas. In rats, the NADPH diaphorase activity of amacrine and horizontal cells exhibited adaptation dependency similar to that of the rabbit retina. But, the most pronounced effect of dark adaptation in the rat's retina was an enhancement of NADPH diaphorase activity in Müller cells, especially of the endfoot region. Assuming that NADPH diaphorase activity is a marker for NOS, these findings suggest that NO production in the mammalian retina is modulated by the level of ambient illumination and support the notion that NO plays a physiological role in the retina.
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Miller, N., R. Saada, S. Markovich, I. Hurwitz, and A. J. Susswein. "l-arginine via nitric oxide is an inhibitory feedback modulator of Aplysia feeding." Journal of Neurophysiology 105, no. 4 (April 2011): 1642–50. http://dx.doi.org/10.1152/jn.00827.2010.
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An increase in l-arginine hemolymph concentration acts as a postingestion signal inhibiting Aplysia feeding. At physiological concentrations (a 10-μM increase over background), the inhibitory effect of l-arginine is too weak to block feeding in hungry animals. However, a 10-μM increase in l-arginine concentration acts along with another inhibitory stimulus, the sustained presence of food odor, to inhibit feeding after a period of access to food. A physiological concentration of l-arginine also blocked the excitatory effect of a stimulus enhancing feeding, pheromones secreted by mating conspecifics. High concentrations of l-arginine (2.5 mM) alone also inhibited ad libitum feeding. l-arginine is the substrate from which nitric oxide synthase (NOS) produces nitric oxide (NO). Both an NO donor and a 10-μM increase in l-arginine inhibited biting in response to a weak food stimulus. Treatment with NOS inhibitors initiated food-finding and biting in the absence of food, indicating that food initiates feeding against a background of tonic nitrergic inhibition. Increased feeding in response to blocking NOS is accompanied by firing of the metacerebral (MCC) neuron, a monitor of food arousal. The excitatory effect on the MCC of blocking NOS is indirect. The data suggest that l-arginine acts by amplifying NO synthesis, which acts as a background stimulus inhibiting feeding. Background modulation of neural activity and behavior by NO may also be present in other systems, but such modulation may be difficult to identify because its effects are evident only in the context of additional stimuli modulating behavior.
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Henson, Sarah E., Timothy C. Nichols, V. Michael Holers, and David R. Karp. "The Ectoenzyme γ-Glutamyl Transpeptidase Regulates Antiproliferative Effects of S-Nitrosoglutathione on Human T and B Lymphocytes." Journal of Immunology 163, no. 4 (August 15, 1999): 1845–52. http://dx.doi.org/10.4049/jimmunol.163.4.1845.
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Abstract Expression of the ectoenzyme γ-glutamyl transpeptidase (GGT) is regulated on T lymphocytes. It is present at a low level on naive T cells, at a high level on activated T cells, and at an intermediate level on resting memory T cells. GGT cleaves the glutamyl group from glutathione, which is the first step in the uptake of extracellular glutathione. In vitro, purified GGT also metabolizes the naturally occurring nitrosothiol, S-nitrosoglutathione (GSNO). Because of this relationship, the effects of cellular GGT on the metabolism of and cellular response to GSNO were tested. The GGT-negative lymphoblasts Ramos and SupT1 were transfected with cDNA for human GGT. In the presence of cells lacking GGT, GSNO is extremely stable. In contrast, GGT-expressing cells rapidly metabolize GSNO leading to nitric oxide release. The nitric oxide causes a rapid (<2-h) inhibition of DNA synthesis. There is a concomitant decrease in the concentration of intracellular deoxyribonucleotides, suggesting that one effect of the nitric oxide generated from GSNO is the previously described inactivation of the enzyme ribonucleotide reductase. GSNO also caused a rapid, GGT-dependent cytostatic effect in Hut-78, a human T cell lymphoma, as well as in activated peripheral blood T cells. Although DNA synthesis was decreased to 16% of control values in anti-CD3-stimulated Hut-78, the production of IL-2 was unchanged by GSNO. These data show that GGT, a regulated ectoenzyme on T cells, controls the rate of nitric oxide production from GSNO and thus markedly affects the physiological response to this biologically active nitrosothiol.