Alpha-Melanocyte-Stimulating Hormone through Melanocortin-4 Receptor Inhibits Nitric Oxide Synthase and Cyclooxygenase Expression in the Hypothalamus of Male Rats

2004 ◽  
Vol 79 (5) ◽  
pp. 278-286 ◽  
Author(s):  
Carla Caruso ◽  
Claudia Mohn ◽  
Armando L. Karara ◽  
Valeria Rettori ◽  
Hajime Watanobe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Male Rats ◽  
Melanocyte Stimulating Hormone ◽  
Melanocortin 4 Receptor ◽  
Oxide Synthase ◽  
Stimulating Hormone

Abstract 15295: Molecular Mechanism of Chronic Sildenafil-Caused Regression of Heart Failure: Effects on the Express of Cardiac SR Ca2+-ATPase, Subtype of β-Adrenergic Receptors and Nitric Oxide Synthase Isoforms

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Heng-Jie Cheng ◽  
Tiankai Li ◽  
Che Ping Cheng
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Adrenergic Receptors ◽  
Left Ventricular ◽  
Male Rats ◽  
Protein Levels ◽  
Myocyte Function ◽  
Oxide Synthase ◽  
Β Adrenergic Receptors

Background: Sildenafil (SIL), a selective inhibitor of PDE5 has been shown to exert profound beneficial effects in heart failure (HF). Recently we further found that SIL caused regression of cardiac dysfunction in a rat model with isoproterenol (ISO)-induced progressive HF. However, the molecular basis is unclear. We hypothesized that reversal of HF-induced detrimental alterations on the expressions of cardiac SR Ca 2+ -ATPase (SERCA2a), β-adrenergic receptors (AR) and nitric oxide synthase (NOS) isoforms by SIL may play a key role for its salutary role in HF. Methods: Left ventricular (LV) and myocyte function and the protein levels of myocyte β 1 - and β 3 - AR, SERCA2a, phospholamban (PLB) and three NOS were simultaneously evaluated in 3 groups of male rats (6/group): HF , 3 months (M) after receiving ISO (170 mg/kg sq for 2 days); HF/SIL , 2 M after receiving ISO, SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and Controls (C). Results: Compared with controls, ISO-treated rats progressed to severe HF at 3 M after ISO followed by significantly decreased LV contractility (E ES , HF: 0.7 vs C: 1.2 mmHg/μl) and slowed LV relaxation, reductions in the peak velocity of myocyte shortening (77 vs 136 μm/sec), relengthening (62 vs 104 μm/sec) and [Ca 2+ ] iT (0.15 vs 0.24) accompanied by a diminished myocyte inotropic response to β-AR agonist, ISO (10 -8 M). These abnormalities were associated with concomitant significant decreases in myocyte protein levels of β 1 -AR (0.23 vs 0.64), SERCA2a (0.46 vs 0.80), PLB Ser16 /PLB ratio (0.24 vs 0.40) and eNOS (0.28 vs 0.46), but significantly increases in protein levels of β 3 -AR (0.29 vs 0.10) and iNOS (0.18 vs 0.08) with relatively unchanged nNOS. Chronic SIL prevented the HF-induced decreases in LV and myocyte contraction, relaxation, peak [Ca 2+ ] iT , and restored normal myocyte contractile response to ISO stimulation. With SIL, protein levels of myocyte β 1 - and β 3 -AR, SERCA2a were restored close to control values, but eNOS was significantly elevated than controls (0.77). Conclusions: Chronic SIL prevents HF-caused downregulation of cardiac β 1 -AR and reverse contrast changes between iNOS and β 3 -AR with SERCA 2a and eNOS expression, leading to the preservation of LV and myocyte function, [Ca 2+ ] iT , and β-adrenergic reserve.

scholarly journals Effect of Goat Milk Yogurt for Prevention Hypercholesterolamic in Animal Model Rat (Rattus norvegius) Based on the Expression of Inducible Nitric Oxide Synthase (INOS) and a description of Liver Histopathology

2017 ◽  
Vol 7 (2) ◽  
pp. 38
Author(s):  
Chanif Mahdi ◽  
Sukarno Hariyanto ◽  
Masdiana C. Pandaga
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Goat Milk ◽  
Male Rats ◽  
Ldl Oxidation ◽  
Preventive Action ◽  
Liver Histopathology ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The pattern of high consumption of fat can lead to hypercholesterolemia were accompanied by increased levels of LDL which resulted in LDL oxidation, accompanied by an inflammatory reaction that can lead to liver tissue damage resulting in increased expression of inducible Nitric Oxide Synthase (INOS) and changes in liver histopathology. The purpose of this study was to investigate the influence of goat milk yogurt supplementation on the expression of INOS and liver histopathology picture. This study used 20 male rats, Wistar strain aged 10-12 weeks, weighing 150-200g. Giving goat milk yogurt for 42 days with a dose of 300mg/kg, 600mg/kg, and 900mg/kg and giving dietary hypercholesterolemia by administering poached quail egg yolk, lard, and cholic acid by the stomach sonde for 14 days. Parameters measured were the expression of INOS and liver histopathology picture. The analysis used in this study is the One Way Analysis Of Variance (ANOVA) followed by Tukey test 5%. The results showed that administration of goat milk yogurt as a precaution hypercholesterolemia at a dose of 300mg/kg, 600mg/kg and 900mg/kg give a highly significant effect (p <0.01) on the expression of INOS (p <0.01).The overall Result of each treatment were 0.47 ±0.03; 6.72 ± 0.11; 2.40 ±0.16;1.11 ±0.07and 0.66 ±0.19  Prevention with a dose of 900 mg/kg body weight is the most effective dose inhibits the expression of INOS.  Prevention with a dose of 900 mg/kg showed that the histopathological picture of approaching normal circumstances. The conclusion of the study is the provision of goat milk yogurt as a preventive action with a dose of 900 mg/kg of the most effective to inhibit the expression of INOS and maintain normal liver histology in rats given diets hypercholesterolemia.Keywords: Hypercholesterolemia, Expression of Inducible Nitric Oxide Synthase (INOS), goat's milk yogurt, liver histopathology

scholarly journals INHIBITION OF TRANSCRIPTION FACTORS NF KAPPA B AND AP-1 LIMITS THE PROGRESSION OF OXIDATIVE-NITROSATIVE STRESS IN THE TISSUE OF CEREBRAL HEMISPHERES IN RATS AFTER MODELLED TRAUMATIC BRAIN INJURY

2020 ◽  
Vol 20 (1) ◽  
pp. 80-85 ◽  
Author(s):  
I.V. Yavtushenko ◽  
V.O. Kostenko
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Transcription Factors ◽  
Brain Injury ◽  
Nitric Oxide Synthase ◽  
Nitrosative Stress ◽  
Cerebral Hemispheres ◽  
Male Rats ◽  
Nf Kappa B ◽  
Oxide Synthase

The study was aimed as investigating the effects of inhibitors of transcription factors NF kappa B and AP-1 activation on the development of oxidative-nitrosative stress in rat cerebral hemispheres following experimental traumatic brain injury (TBI). The study included 60 white Wistar male rats weighing 180-220 g, divided into 4 groups of 7 animals in each: the 1st group included pseudo-injured animals subjected to the same manipulations (ether anaesthesia, fixation) as the animals  in the experimental groups, except for TBI modelling, the 2nd group included the animals exposed to modelled TBI, the 3rd and 4th groups involved the rats who received ammonium pyrolidine dithiocarbamate, the nuclear translocation inhibitor NF kappa B in a dose of 76 mg/kg and the inhibitor AP-1 SR 11302 in a dose of 1 mg/kg, respectively for 7 days following the TBI modelling. On the 7th day after the simulation of a moderate TBI in rat cerebral hemisphere tissue, the following signs of oxidative-nitrosative stress have been detected: increased production of superoxide radical anion by NADPH and NADH-dependent electron transport chains, increased activity of nitric oxide synthase (total and inducible), a decrease and impairment of the coupling of its constitutive isoform, growth in the concentration of peroxynitrite, the development of decompensated lipid peroxidation. The application of transcription factor inhibitors NF kappa B (PDTC) and AP-1 (SR 11302) significantly reduces the signs of oxidative-nitrosative stress in the tissue of rat cerebral hemispheres on the 7th day of the experiment, reduces the production of superoxide anion radical and the activity of nitric oxide synthase (total and inducible), improves the coupling of its constitutive isoform, limits the peroxynitrite concentration, and enhances the antioxidant potential.

Prolactin promotes oxytocin and vasopressin release by activating neuronal nitric oxide synthase in the supraoptic and paraventricular nuclei

2010 ◽  
Vol 299 (6) ◽  
pp. R1701-R1708 ◽  
Author(s):  
Claudia Vega ◽  
Bibiana Moreno-Carranza ◽  
Miriam Zamorano ◽  
Andrés Quintanar-Stéphano ◽  
Isabel Méndez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Anterior Pituitary ◽  
Neuronal Nitric Oxide Synthase ◽  
Male Rats ◽  
Female Reproduction ◽  
Vasopressin Release ◽  
Hypothalamic Nuclei ◽  
Pituitary Glands ◽  
Oxide Synthase

Prolactin (PRL) stimulates the secretion of oxytocin (OXT) and arginine AVP as part of the maternal adaptations facilitating parturition and lactation. Both neurohormones are under the regulation of nitric oxide. Here, we investigate whether the activation of neuronal nitric oxide synthase (nNOS) in the hypothalamo-neurohypophyseal system mediates the effect of PRL on OXT and AVP release and whether these effects operate in males. Plasma levels of OXT and AVP were measured in male rats after the intracerebroventricular injection of PRL or after inducing hyperprolactinemia by placing two anterior pituitary glands under the kidney capsule. NOS activity was evaluated in the paraventricular (PVN) and supraoptic (SON) hypothalamic nuclei by NADPH-diaphorase histochemistry and in hypothalamic extracts by the phosphorylation/inactivation of nNOS at Ser847. Elevated central and systemic PRL correlated with increased NOS activity in the PVN and SON and with higher OXT and AVP circulating levels. Notably, treatment with 7-nitroindazole, a selective inhibitor of nNOS, prevented PRL-induced stimulation of the release of both neurohormones. Also, phosphorylation of nNOS was reduced in hyperprolactinemic rats, and treatment with bromocriptine, an inhibitor of anterior pituitary PRL secretion, suppressed this effect. These findings suggest that PRL enhances nNOS activity in the PVN and SON, thereby contributing to the regulation of OXT and AVP release. This mechanism likely contributes to the regulation of processes beyond those of female reproduction.

Hippocampal neuronal nitric oxide synthase (nNOS) is regulated by nicotine and stress in female but not in male rats

2011 ◽  
Vol 1368 ◽  
pp. 134-142 ◽  
Author(s):  
Aysegul Keser ◽  
Burcu Balkan ◽  
Oguz Gozen ◽  
Lutfiye Kanit ◽  
Sakire Pogun
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Male Rats ◽  
Oxide Synthase
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