scholarly journals Role of endogenous nitric oxide on PAF-induced vascular and respiratory effects

1995 ◽  
Vol 4 (2) ◽  
pp. 124-129 ◽  
Author(s):  
M. Clement ◽  
M. Albertini
Keyword(s):  
Nitric Oxide ◽  
Cardiac Activity ◽  
Hypotensive Effect ◽  
Synthesis Inhibitor ◽  
Mechanically Ventilated ◽  
Respiratory Effects ◽  
Basal Tone ◽  
Before And After ◽  
Endogenous Nitric Oxide

The role of endogenous nitric oxide (NO) on vascular and respiratory smooth muscle basal tone was evaluated in six anaesthetized, paralysed, mechanically ventilated pigs. The involvement of endogenous NO in PAF-induced shock and airway hyperresponsiveness was also studied. PAF (50 ng/kg, i.v.) was administered before and after pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg, i.v.), an NO synthesis inhibitor. PAF was also administered to three of these pigs after indomethacin infusion (3 mg/kg, i.v.). In normal pigs, L-NAME increased systemic and pulmonary vascular resistances, caused pulmonary hypertension and reduced cardiac output and stroke volume. The pulmonary vascular responses were correlated with the increase in static and dynamic lung elastances, without changing lung resistance. Inhibition of NO synthesis enhanced the PAF-dependent increase in total, intrinsic and viscoelastic lung resistances, without affecting lung elastances or cardiac activity. The systemic hypotensive effect of PAF was not abolished by pretreatment with L-NAME or indomethacin. This indicates that systemic hypotension is not correlated with the release of endogenous NO or prostacyclines. Indomethacin completely abolished the PAF-dependent respiratory effects.

Endogenous nitric oxide modulates responses of tissue and airway resistance to vagal stimulation in piglets

2002 ◽  
Vol 93 (2) ◽  
pp. 450-456 ◽  
Author(s):  
Mohammad Y. Khassawneh ◽  
Ismail A. Dreshaj ◽  
Shijian Liu ◽  
Chung-Ho Chang ◽  
Musa A. Haxhiu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Airway Resistance ◽  
Vagal Stimulation ◽  
No Synthase ◽  
Excitatory Response ◽  
Tissue Resistance ◽  
Before And After ◽  
Endogenous Nitric Oxide ◽  
Cholinergic Effects

The role of endogenous nitric oxide (NO) in modulating the excitatory response of distal airways to vagal stimulation is unknown. In decerebrate, ventilated, open-chest piglets aged 3–10 days, lung resistance (Rl) was partitioned into tissue resistance (Rti) and airway resistance (Raw) by using alveolar capsules. Changes in Rl, Rti, and Raw were evaluated during vagal stimulation at increasing frequency before and after NO synthase blockade with N ω-nitro-l-arginine methyl ester (l-NAME). Vagal stimulation increased Rl by elevating both Rti and Raw. NO synthase blockade significantly increased baseline Rti, but not Raw, and significantly augmented the effects of vagal stimulation on both Rti and Raw. Vagal stimulation also resulted in a significant increase in cGMP levels in lung tissue before, but not after, l-NAME infusion. In seven additional piglets after Rl was elevated by histamine infusion in the presence of cholinergic blockade with atropine, vagal stimulation failed to elicit any change in Rl, Rti, or Raw. Therefore, endogenous NO not only plays a role in modulating baseline Rti, but it opposes the excitatory cholinergic effects on both the tissue and airway components of Rl. We speculate that activation of the NO/cGMP pathway during cholinergic stimulation plays an important role in modulating peripheral as well as central contractile elements in the developing lung.

Role of endothelium-derived nitric oxide in hemodynamic adaptations after graded renal mass reduction

1993 ◽  
Vol 264 (6) ◽  
pp. R1254-R1259 ◽  
Author(s):  
K. A. Griffin ◽  
A. K. Bidani ◽  
J. Ouyang ◽  
V. Ellis ◽  
M. Churchill ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Mass ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Mass Reduction ◽  
Synthesis Inhibitor ◽  
Contralateral Kidney ◽  
Before And After ◽  
Renal Vascular

The mediator(s) of the adaptive increases in renal blood flow (RBF) and glomerular filtration rate (GFR) after renal mass reduction have not been identified. The present studies were designed to investigate the role of endothelium-derived nitric oxide (EDNO) in the hemodynamic adaptations after graded renal mass reduction. The experiments were performed in rats that had undergone a sham reduction in renal mass, uninephrectomy (UNX), or 5/6 NX (UNX plus excision of both poles of the contralateral kidney) 3-4 wk before. Measurements of RBF, GFR, renal vascular resistance (RVR), mean arterial pressure (MAP), and plasma renin concentration (PRC) were obtained before and after administration of the EDNO synthesis inhibitor NG-monomethyl-L-arginine (L-NMMA). L-NMMA (50 mg/kg bolus plus 500 micrograms.kg-1.min-1 infusion) led to significant (P < 0.01) and comparable increases in MAP (mmHg) (P < 0.01) in sham rats (117 +/- 6 to 154 +/- 6), UNX rats (112 +/- 5 to 139 +/- 7), and 5/6 NX rats (116 +/- 5 to 149 +/- 7). RVR increased significantly in all three groups (P < 0.01). The resultant decrease in RBF (ml.min-1.kg-1) was similar in sham rats (34.9 +/- 2.6 to 23.8 +/- 1.6), UNX rats (43.9 +/- 3.6 to 27.3 +/- 2.8), and 5/6 NX rats (34.6 +/- 2 to 22.3 +/- 1.6) (P < 0.01 for all groups).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Role of endogenous nitric oxide (NO) and NO synthases in healing of indomethacin-induced intestinal ulcers in rats

Life Sciences ◽  
2007 ◽  
Vol 80 (4) ◽  
pp. 329-336 ◽  
Author(s):  
Koji Takeuchi ◽  
Ryo Hatazawa ◽  
Mayu Tanigami ◽  
Akiko Tanaka ◽  
Ryoko Ohno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endogenous Nitric Oxide ◽  
Intestinal Ulcers

Nitric oxide: a new role in intensive care

2020 ◽  
Vol 22 (1) ◽  
pp. 72-79
Author(s):  
Alexandra Lee ◽  
◽  
Warwick Butt ◽  
◽  
◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Potential Role ◽  
Nitric Oxide Donors ◽  
Ischaemia Reperfusion Injury ◽  
Surface Receptors ◽  
The Past ◽  
Ischaemia Reperfusion ◽  
Human Experiments ◽  
Endogenous Nitric Oxide

Inhaled nitric oxide has been used for 30 years to improve oxygenation and decrease pulmonary vascular resistance. In the past 15 years, there has been increased understanding of the role of endogenous nitric oxide on cell surface receptors, mitochondria, and intracellular processes involving calcium and superoxide radicals. This has led to several animal and human experiments revealing a potential role for administered nitric oxide or nitric oxide donors in patients with systemic inflammatory response syndrome or ischaemia–reperfusion injury, and in patients for whom exposure of blood to artificial surfaces has occurred.

scholarly journals Serum levels of NG, NG-dimethyl-L-arginine, a potential endogenous nitric oxide inhibitor in dialysis patients.

1997 ◽  
Vol 8 (9) ◽  
pp. 1437-1442
Author(s):  
B Anderstam ◽  
K Katzarski ◽  
J Bergström
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Serum Levels ◽  
Model Systems ◽  
Dialysis Dose ◽  
Control Subjects ◽  
Before And After ◽  
Endogenous Nitric Oxide ◽  
Experimental Model Systems ◽  
The One

Nitric oxide (NO) is involved in blood pressure regulation, and its synthesis is inhibited by methylarginines. It has been hypothesized that one of these, asymmetrical dimethylarginine (ADMA), may contribute to dialysis-associated hypertension because it accumulates in the plasma of hemodialysis (HD) patients in a concentration high enough (4 mumol/L) to inhibit NO synthesis in experimental model systems. A precolumn HPLC technique was used to quantify methylarginines (ADMA and symmetrical dimethylarginine [SDMA]) in plasma from HD patients before and after dialysis, from continuous ambulatory peritoneal dialysis (CAPD) patients, and from healthy subjects. Plasma ADMA concentrations were 0.59 +/- 0.22 (SD) mumol/L in HD patients predialysis (n = 19) and 0.70 +/- 0.27 mumol/L in CAPD patients (n = 11), versus about half of the concentration in control subjects (0.36 +/- 0.08 mumol/L, n = 7). The concentrations of SDMA (not an inhibitor of NO formation) were approximately four to five times the ADMA concentrations in both HD and CAPD patients, in contrast to a ratio of 1:1 in the control subjects. Methylarginine concentrations were reduced by 23% and 40% postdialysis, as calculated from ADMA and SDMA values, respectively. No significant correlations were observed between ADMA concentrations, on the one had, and blood pressure, creatinine and dialysis dose (Kt/V urea), on the other hand. It is concluded that plasma levels of ADMA are considerably lower than those reported earlier in patients treated with HD and also below the levels that hitherto have been thought to have clinical relevance. The role of ADMA in inhibiting NO in dialysis-associated hypertension is questioned.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

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