Role of Nitric Oxide in the Enhancement of Pentylenetetrazole-Induced Seizures Caused by Shigella dysenteriae

1999 ◽  
Vol 67 (12) ◽  
pp. 6364-6368 ◽  
Author(s):  
Judith Balter-Seri ◽  
Yael Yuhas ◽  
Abraham Weizman ◽  
Yehuda Nofech-Mozes ◽  
Elizabeth Kaminsky ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Potent Inhibitor ◽  
Elevated Serum ◽  
Selective Inhibitor ◽  
No Synthase ◽  
Shigella Dysenteriae ◽  
Contrast Injection ◽  
The Mean

ABSTRACT Convulsions and encephalopathy are frequent complications of childhood shigellosis. We studied the role of nitric oxide (NO) inShigella-related seizures in an animal model. Pretreatment of mice with Shigella dysenteriae 60R sonicate elevated serum NO levels and enhanced the convulsive response to pentylenetetrazole (PTZ), as indicated by a higher mean convulsion score and a higher number of mice responding with seizures. Treatment of the mice with S-methylisothiourea sulfate (SMT), a potent inhibitor of inducible NO synthase (NOS), prevented the elevation of serum NO levels and concomitantly reduced the enhanced response to PTZ. The mean convulsion scores were 0.7, 0.7, 1.3, and 0.8 for mice treated with saline, saline and SMT, S. dysenteriae 60R sonicate, and S. dysenteriae60R sonicate with SMT, respectively (P = 0.001 for 60R sonicate versus saline and P = 0.013 for 60R sonicate versus 60R sonicate with SMT). The corresponding seizure rates were 40, 44, 75, and 47% for saline, saline with SMT, S. dysenteriae 60R sonicate, and S. dysenteriae 60R sonicate with SMT, respectively (P = 0.0004 for 60R sonicate versus saline and P = 0.005 for 60R sonicate versus 60R sonicate with SMT). In contrast, injection of N-nitro-l-arginine, a selective inhibitor of constitutive NOS, neither abolished the elevation of serum NO nor attenuated the enhancement of seizures. These findings indicate that NO, induced by S. dysenteriae 60R sonicate, is involved in enhancing the susceptibility to seizures caused by S. dysenteriae.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

scholarly journals Protective Role of Leptadenia Hastata on the Haematological and Biochemical Alterations in Adrenaline-Induced Hypertensive Rats

2020 ◽  
Vol 14 (1) ◽  
pp. 25-32
Author(s):  
Adewuyi Hassan Abdulsalam ◽  
◽  
Muhammad L. Hadiza ◽  
Onukogu Stella Chiamaka ◽  
Ibrahim Jonathan ◽  
...  
Keyword(s):  
Elevated Serum ◽  
Protective Role ◽  
Protective Effects ◽  
Hypertensive Rats ◽  
Bioactive Constituents ◽  
Once Daily ◽  
Biochemical Alterations ◽  
The Mean ◽  
Normal Controls

Background: Leptadenia hastata (L. Hastata) is a plant used for various diseases in Nigeria. This study evaluated the protective effects of L. hastate on the haematological and biochemical alterations in adrenaline-induced hypertensive rats. Methods: Twenty-five rats were divided equally into five groups (A-E). Groups A-D were given 0.5 mg/kg adrenaline, groups A and B were treated with 100 and 200 mg/kg the extract of L. Hastata, respectively, while groups C and D were treated with 5 mg/kg amlodipine (standard control) and normal saline (untreated control), respectively. Group E were given distilled water (normal controls). The adrenaline was injected intraperitoneally while the extract was given orally once daily for seven days. Results: Treatment with 100 and 200 mg/kg of the extract significantly reduced the elevated serum albumin, ALP, ALT, AST, chloride, sodium and creatinine, cholesterol and LDL concentrations compared with the untreated hypertensive rats. The bicarbonate level, WBC and RBC counts, mean cell hemoglobin and packed cell value were higher in rats treated with the extract compared with the untreated hypertensive rats. The mean cell value, HDL, triglyceride, urea, potassium, total and direct bilirubin concentrations in experimental groups were not significantly different from those in the controls (P<0.05). Conclusion: Our results suggest that treatment of the hypertensive rats with the extract of L. Hastata protects against renal, hepatic and cardiac damages, thus it could be considered as a natural anti-hypertensive agent. Further studies are required to identify the bioactive constituents and the mechanism(s) of action.

Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules

1997 ◽  
Vol 272 (6) ◽  
pp. H2541-H2546 ◽  
Author(s):  
G. Dornyei ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Thromboxane A2 ◽  
No Synthase ◽  
Gracilis Muscle ◽  
Vasoactive Agents ◽  
Before And After ◽  
Higher Doses

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

Is nitric oxide the final mediator regulating the migrating myoelectric complex cycle?

1995 ◽  
Vol 268 (2) ◽  
pp. G207-G214 ◽  
Author(s):  
A. Rodriguez-Membrilla ◽  
V. Martinez ◽  
M. Jimenez ◽  
E. Gonalons ◽  
P. Vergara
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Motor Pattern ◽  
No Synthase ◽  
Phase Iii ◽  
Motor Patterns ◽  
No Donor ◽  
Postprandial State ◽  
Synthase Inhibitor

The main objective was to study the role of nitric oxide (NO) in the conversion of migrating myoelectric complexes (MMC) to the irregular electrical activity characteristic of the postprandial state. Both rats and chickens were implanted with electrodes for electromyography in the small intestine. Intravenous infusion of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, induced an organized MMC-like pattern in fed rats. Infusion of sodium nitroprusside, a NO donor, disrupted the MMC, inducing a postprandial-like motor pattern in fasting rats. Similarly, in chickens L-NNA mimicked the fasting pattern, consisting of a shortening of phase II, enlargement of phase III, orad displacement of the origin of the MMC, and an increase in the speed of phase III propagation. An inhibition of NO synthesis seems to be involved in the induction of the fasting motor pattern, whereas an increase of NO mediates the occurrence of the fed pattern. It is suggested that NO might be the final mediator in the control of small intestine motor patterns.

Compensatory role of NO in cerebral circulation of piglets chronically treated with indomethacin

2002 ◽  
Vol 282 (2) ◽  
pp. R400-R410 ◽  
Author(s):  
Yifan Zhang ◽  
C. W. Leffler
Keyword(s):  
Nitric Oxide ◽  
Cerebrospinal Fluid ◽  
Methyl Ester ◽  
Cerebral Circulation ◽  
No Synthase ◽  
Inhibitory Effects ◽  
Circulatory Control ◽  
Pial Arterioles ◽  
Indomethacin Treatment

We hypothesize that inhibitory effects exist between prostanoids and nitric oxide (NO) in their contributions to cerebral circulation. Piglets (1–4 days old) were divided into three chronically treated (6–8 days) groups: control piglets, piglets treated with indomethacin (75 mg/day), and piglets treated with N ω-nitro-l-arginine methyl ester (l-NAME, 100 mg · kg−1 · day−1). Pial arterioles dilated in response to hypercapnia similarly among the three groups (41 ± 4, 40 ± 6, and 45 ± 11%). Cerebrospinal fluid cAMP increased in control piglets, while cGMP increased in indomethacin-treated piglets. l-NAME, but not 7-nitroindazole, inhibited the response to hypercapnia only in indomethacin-treated piglets (40 ± 6 vs. 17 ± 5%). Topical sodium nitroprusside or iloprost restored dilation in response to hypercapnia. Similar results were obtained when the dilator was bradykinin. Pial arterioles of control and l-NAME-treated piglets constricted in response to ACh (−24 ± 3%). However, those of indomethacin-treated piglets dilated in response to ACh (15 ± 2%). This dilation was inhibited by l-NAME. NO synthase activity, but not endothelial NO synthase expression, increased after chronic indomethacin treatment. These data suggest that chronic inhibition of cyclooxygenase can increase the contribution of NO to cerebrovascular circulatory control in piglets.

scholarly journals Nitric Oxide and the Neuroendocrine Control of the Osmotic Stress Response in Teleosts

2019 ◽  
Vol 20 (3) ◽  
pp. 489 ◽  
Author(s):  
Carla Cioni ◽  
Elisa Angiulli ◽  
Mattia Toni
Keyword(s):  
Nitric Oxide ◽  
Stress Response ◽  
Osmotic Stress ◽  
No Synthase ◽  
Hormone Release ◽  
Neurosecretory Neurons ◽  
Osmotic Stress Response ◽  
Osmotic Challenge ◽  
Osmotic Stimuli

The involvement of nitric oxide (NO) in the modulation of teleost osmoresponsive circuits is suggested by the facts that NO synthase enzymes are expressed in the neurosecretory systems and may be regulated by osmotic stimuli. The present paper is an overview on the research suggesting a role for NO in the central modulation of hormone release in the hypothalamo-neurohypophysial and the caudal neurosecretory systems of teleosts during the osmotic stress response. Active NOS enzymes are constitutively expressed by the magnocellular and parvocellular hypophysiotropic neurons and the caudal neurosecretory neurons of teleosts. Moreover, their expression may be regulated in response to the osmotic challenge. Available data suggests that the regulatory role of NO appeared early during vertebrate phylogeny and the neuroendocrine modulation by NO is conservative. Nonetheless, NO seems to have opposite effects in fish compared to mammals. Indeed, NO exerts excitatory effects on the electrical activity of the caudal neurosecretory neurons, influencing the amount of peptides released from the urophysis, while it inhibits hormone release from the magnocellular neurons in mammals.

Nitric oxide mediates mitogenic effect of VEGF on coronary venular endothelium

1996 ◽  
Vol 270 (1) ◽  
pp. H411-H415 ◽  
Author(s):  
L. Morbidelli ◽  
C. H. Chang ◽  
J. G. Douglas ◽  
H. J. Granger ◽  
F. Ledda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Growth Factor ◽  
No Synthase ◽  
Mitogenic Effect ◽  
Microvascular Endothelium ◽  
Proliferative Effect

Vascular endothelial growth factor (VEGF) is a secreted protein that is a specific growth factor for endothelial cells. We have recently demonstrated that nitric oxide (NO) donors and vasoactive peptides promoting NO-mediated vasorelaxation induce angiogenesis in vivo as well as endothelial cell growth and motility in vitro; in contrast, inhibitors of NO synthase suppress angiogenesis. In this study we investigated the role of NO in mediating the mitogenic effect of VEGF on cultured microvascular endothelium isolated from coronary postcapillary venules. VEGF induced a dose-dependent increase in cell proliferation and DNA synthesis. The role of NO was determined by monitoring proliferation or guanosine 3',5'-cyclic monophosphate (cGMP) levels in the presence and absence of NO synthase blockers. The proliferative effect evoked by VEGF was reduced by pretreatment of the cells with NO synthase inhibitors. Exposure of the cells to VEGF induced a significant increment in cGMP levels. This effect was potentiated by superoxide dismutase addition and was abolished by NO synthase inhibitors. VEGF stimulates proliferation of postcapillary endothelial cells through the production of NO and cGMP accumulation.

scholarly journals Autoregulatory Role of Endothelium-derived Nitric Oxide (NO) on Lipopolysaccharide-induced Vascular Inducible NO Synthase Expression and Function

2004 ◽  
Vol 280 (8) ◽  
pp. 7236-7243 ◽  
Author(s):  
Phuong A. Vo ◽  
Bhavini Lad ◽  
James A. P. Tomlinson ◽  
Stephanie Francis ◽  
Amrita Ahluwalia
Keyword(s):  
Nitric Oxide ◽  
No Synthase ◽  
Inducible No Synthase ◽  
And Function
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