scholarly journals Increased nitric oxide activity in a rat model of acute pancreatitis

Gut ◽  
1998 ◽  
Vol 43 (4) ◽  
pp. 564-570 ◽  
Author(s):  
R A Al-Mufti ◽  
R C N Williamson ◽  
R T Mathie
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Acute Pancreatitis ◽  
Arterial Blood Pressure ◽  
Tissue Damage ◽  
No Synthase ◽  
Arterial Blood ◽  
Inducible No Synthase ◽  
Cellular Localisation ◽  
Male Wistar Rats

Background—Overproduction of nitric oxide (NO) via induction of the inducible NO synthase (iNOS) is an important factor in the haemodynamic disturbances of several inflammatory states.Aims—To identify the role of NO in a caerulein induced model of acute pancreatitis in the rat.Methods—Arterial blood pressure and plasma NO metabolites were measured at zero and seven hours in adult male Wistar rats administered caerulein (n=10) or saline (n=10). Pancreatic activity of NOS (inducible and constitutive) was assayed biochemically. The pancreatic expression and cellular localisation of NOS and nitrotyrosine (a marker of peroxynitrite induced oxidative tissue damage) were characterised immunohistochemically.Results—Compared with controls at seven hours, the pancreatitis group displayed raised plasma NO metabolites (mean (SEM) 70.2 (5.9) versus 22.7 (2.2) μmol/l, p<0.0001) and reduced mean arterial blood pressure (88.7 (4.6) versus 112.8 (4.1) mm Hg, p=0.008). There was notable iNOS activity in the pancreatitis group (3.1 (0.34) versus 0.1 (0.01) pmol/mg protein/min, p<0.0001) with reduced constitutive NOS activity (0.62 (0.12) versus 0.96 (0.08) pmol/mg protein/min, p=0.031). The increased expression of iNOS was mainly localised within vascular smooth muscle cells (p=0.003 versus controls), with positive perivascular staining for nitrotyrosine (p=0.0012 versus controls).Conclusions—In this experimental model of acute pancreatitis, iNOS induction and oxidative tissue damage in the pancreas is associated with raised systemic NO and arterial hypotension. Excess production of NO arising from the inducible NO synthase may be an important factor in the systemic and local haemodynamic disturbances associated with acute pancreatitis.

scholarly journals Cerebral Blood Flow Changes during Cortical Spreading Depression are Not Altered by Inhibition of Nitric Oxide Synthesis

1994 ◽  
Vol 14 (6) ◽  
pp. 939-943 ◽  
Author(s):  
Zheng Gang Zhang ◽  
Michael Chopp ◽  
Kenneth I. Maynard ◽  
Michael A. Moskowitz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Arterial Blood ◽  
Nos Inhibitors ◽  
Before And After ◽  
Male Wistar Rats

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-l-arginine (L-NNA) or N-nitro-l-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.

scholarly journals Effects of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor, in L-NAME-induced hypertension in rats

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 57-59 ◽  
Author(s):  
Marcio Wilker Soares Campelo ◽  
Ana Paula Bomfim Soares Campelo ◽  
Luiz Gonzaga de França Lopes ◽  
Armenio Aguiar dos Santos ◽  
Sergio Botelho Guimarães ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Methyl Ester ◽  
Arterial Blood Pressure ◽  
Wistar Rats ◽  
Nitric Oxide Donor ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Male Wistar Rats

PURPOSE: To evaluate the effect of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor in Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. METHODS: Twenty-four male Wistar rats were randomly assigned to four groups (n=6), named according to the treatment applied (G1-Saline, G2-Rut-bpy, G3-L-NAME and G4-L-NAME+Rut-bpy). L-NAME (30 mg/Kg) was injected intraperitoneally 30 minutes before the administration of Rut-bpy (100 mg/Kg). Mean abdominal aorta arterial blood pressure (MAP) was continuously monitored. RESULTS: Mean arterial blood pressure (MAP) in G3 rats rose progressively, reaching 147±16 mmHg compared with 100±19 mm Hg in G1 rats (p<0.05). In G4 rats, treated with L-NAME+Rut-bpy, MAP reached 149+11 mm Hg while in G2 rats, treated with Rut-bpy, MAP values were 106±11 mm Hg. In G1 rats these values decreased progressively reaching 87+14 mm Hg after 30 minutes. An important finding was the maintenance of the MAP throughout the experiment in G2 rats. CONCLUSION: Rut-bpy does not decrease the MAP in L-Name induced hypertensive rats. However, when it is used in anesthetized hypotensive rats a stable blood pressure is obtained.

scholarly journals Chronic Endothelium-Dependent Regulation of Arterial Blood Pressure by Atrial Natriuretic Peptide: Role of Nitric Oxide and Endothelin-1

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2382-2387 ◽  
Author(s):  
Karim Sabrane ◽  
Markus-N. Kruse ◽  
Alexandra Gazinski ◽  
Michaela Kuhn
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Methyl Ester ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP), via its guanylyl cyclase (GC)-A receptor, plays a key role in the regulation of arterial blood pressure (ABP) and volume. Endothelial-restricted deletion of GC-A in mice [endothelial cell (EC) GC-A knockout (KO)] resulted in hypervolemic hypertension, demonstrating that the endothelium participates in the hypotensive and hypovolemic actions of ANP. Published studies showed that ANP modulates the release of the vasoactive factors nitric oxide (NO) and endothelin-1 (ET-1) from cultured endothelia. Based on these observations, we examined the role of these endothelial factors in ANP-dependent vasodilatation (studied in isolated arteries) and chronic regulation of ABP (measured in awake mice by tail-cuff plethysmography). ANP induced concentration-dependent vasorelaxations of aortic, carotid, and pulmonary arteries. These responses were not different between control and EC GC-A KO mice, and were significantly enhanced after inhibition of NO synthase [by N(G)-nitro-l-arginine-methyl ester]. Intravenous administration of N(G)-nitro-l-arginine-methyl ester to conscious mice significantly increased ABP. The extent of these hypertensive reactions was similar in EC GC-A KO mice and control littermates (increases in systolic blood pressure by ∼25 mm Hg). Conversely, antagonism of ET-1/endothelin-A receptors with BQ-123 reduced ABP significantly and comparably in both genotypes (by ∼11 mm Hg). Finally, the vascular and tissue expression levels of components of the NO system and of immunoreactive ET-1 were not different in control and EC GC-A KO mice. We conclude that the endothelium, but not modulation of endothelial NO or ET-1, participates in the chronic regulation of ABP by ANP.

scholarly journals Arterial Blood Pressure Responses to Cell-free Hemoglobin Solutions and the Reaction with Nitric Oxide

1998 ◽  
Vol 273 (20) ◽  
pp. 12128-12134 ◽  
Author(s):  
Ronald J. Rohlfs ◽  
Eric Bruner ◽  
Albert Chiu ◽  
Armando Gonzales ◽  
Maria L. Gonzales ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Free Hemoglobin ◽  
Arterial Blood ◽  
Blood Pressure Responses

scholarly journals The role of l-type calcium channels in the mediation of fast oscillation of arterial blood pressure and renal blood flow in rats

2019 ◽  
Vol 17 (3) ◽  
pp. 253-258
Author(s):  
P. Markova ◽  
R. Girchev
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Experimental Period ◽  
Doppler Probe ◽  
Arterial Blood ◽  
Male Wistar Rats ◽  
Ca2 Channels

The investigation of dynamic characteristics of blood pressure and renal blood flow provides detailed information about the fast regulatory mechanisms involved in arterial blood pressure (ABP) and renal blood flow (RBF) autoregulation. The aim of our study was to investigate the role of L-type Ca2+ channels in the mediation of fast oscillations of arterial blood pressure and renal blood flow in rats by means of spectral analysis. The experiments were performed on anesthetized male Wistar rats (n=7) at the age of 12-14 weeks. The ABP was measured directly in femoral artery; RBF was registered by perivascular ultrasonic Doppler probe (Transonic system) in control and experimental period. The spectrograms from APB and RBF were derived in Lab View 3.11 software. In experimental period the selective L-type Ca2+ channel blocker amlodipine besylate (AML) in dose 200 mkg.kg-1 bolus followed by 50 mkg.kg-1.h infusions was applied. Our results by using a spectral method of analysis of ABP and RBF confirmed involvement of L-type Ca2+ channels in the mediation of dynamic nature of myogenic vascular response. The L-type Ca2+ channels in different specific manner participate in the regulation of renal blood flow and arterial blood pressure.

Does nitric oxide buffer arterial blood pressure variability in humans?

2002 ◽  
Vol 93 (4) ◽  
pp. 1466-1470 ◽  
Author(s):  
William H. Cooke ◽  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
Jian Cui ◽  
Thad E. Wilson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Animal Studies ◽  
Transfer Functions ◽  
Body Position ◽  
Low Frequency ◽  
Power Spectral Analysis ◽  
Arterial Blood

Animal studies suggest that nitric oxide (NO) plays an important role in buffering short-term arterial pressure variability, but data from humans addressing this hypothesis are scarce. We evaluated the effects of NO synthase (NOS) inhibition on arterial blood pressure (BP) variability in eight healthy subjects in the supine position and during 60° head-up tilt (HUT). Systemic NOS was blocked by intravenous infusion of N G-monomethyl-l-arginine (l-NMMA). Electrocardiogram and beat-by-beat BP in the finger (Finapres) were recorded continuously for 6 min, and brachial cuff BP was recorded before and after l-NMMA in each body position. BP and R-R variability and their transfer functions were quantified by power spectral analysis in the low-frequency (LF; 0.05–0.15 Hz) and high-frequency (HF; 0.15–0.35 Hz) ranges.l-NMMA infusion increased supine BP (systolic, 109 ± 4 vs. 122 ± 3 mmHg, P = 0.03; diastolic, 68 ± 2 vs. 78 ± 3 mmHg, P = 0.002), but it did not affect supine R-R interval or BP variability. Beforel-NMMA, HUT decreased HF R-R variability ( P= 0.03), decreased transfer function gain (LF, 12 ± 2 vs. 5 ± 1 ms/mmHg, P = 0.007; HF, 18 ± 3 vs. 3 ± 1 ms/mmHg, P = 0.002), and increased LF BP variability ( P < 0.0001). After l-NMMA, HUT resulted in similar changes in BP and R-R variability compared with tilt without l-NMMA. Increased supine BP afterl-NMMA with no effect on BP variability during HUT suggests that tonic release of NO is important for systemic vascular tone and thus steady-state arterial pressure, but NO does not buffer dynamic BP oscillations in humans.

scholarly journals Inhibition of Nitric Oxide Synthesis: Effects on Cerebral Blood Flow and Glucose Utilisation in the Rat

1993 ◽  
Vol 13 (6) ◽  
pp. 985-992 ◽  
Author(s):  
I. M. Macrae ◽  
D. A. Dawson ◽  
J. D. Norrie ◽  
J. McCulloch
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Bolus Administration ◽  
Nitric Oxide Synthesis ◽  
Conscious Rat ◽  
Nitric Oxide Synthase Inhibitor ◽  
Glucose Utilisation ◽  
Arterial Blood

The consequences of inhibition of nitric oxide synthesis on local CBF and glucose utilisation have been studied in the conscious rat using the specific nitric oxide synthase inhibitor Ng-nitro-l-arginine methyl ester (l-NAME; 30 mg kg−1 i.v.). Local CBF and glucose utilisation were assessed with the [14C]iodoantipyrine and the 2-deoxy-d-[14C]glucose autoradiographic techniques, respectively. l-NAME induced prolonged (>3 h) reductions in local CBF throughout the CNS with concomitant increases in arterial blood pressure. For example, 1 h post l-NAME, CBF dropped from 79 ± 4 to 45 ± 1 ml 100 g−1 min−1 in cerebellum, from 76 ± 4 to 47 ± 2 ml 100 g−1 min−1 in medulla oblongata, and from 117 ± 6 to 72 ± 2 ml 100 g−1 min−1 in cortex. l-NAME produced sustained elevations (e.g., 46 ± 2 mm Hg at 1 h after bolus administration) in mean arterial blood pressure throughout the period evaluated. Despite evidence implicating nitric oxide in neuronal signalling, l-NAME did not significantly influence CNS functional activity, as measured by local rates of glucose utilisation, in any neuroanatomical region examined. Consequently, the normal ratio of blood flow to glucose use throughout the brain was significantly reduced in the presence of l-NAME, although the hierarchy of blood flow levels in different neuroanatomical regions was preserved. These results are consistent with the involvement of nitric oxide in the tonic control of cerebral tissue perfusion.

scholarly journals Role of Endogeneous Nitric Oxide (NO) in Arterial Blood Pressure (ABP) Regulation in Preterm Neonates

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 42A-42A
Author(s):  
Tannette G Krediet ◽  
Leonieke Valk ◽  
Ingrid Hempenius ◽  
Johannes Egberts ◽  
Frank Van Bel
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Preterm Neonates ◽  
Arterial Blood

scholarly journals Hemodynamic evaluation of chemical mediators of sepsis during systemic inflammatory response in an experimental animal model

2021 ◽  
Author(s):  
GUILHERME DE SOUZA VIEIRA ◽  
Fernanda Antunes ◽  
Josias Alves Machado ◽  
Isabella Cristina Morales ◽  
Priscilla Olivieri Benck de Jesus ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Inflammatory Response ◽  
Arterial Blood Pressure ◽  
Cecal Ligation ◽  
Systemic Inflammatory Response ◽  
Arterial Blood ◽  
Time Period ◽  
Sepsis Induction ◽  
Surgical Manipulation

The early diagnosis of sepsis increases the chances of its successful treatment. Biomarkers are able to distinguish between systemic inflammatory response syndrome and sepsis and are used to monitor pro- and anti-inflammatory changes associated with the host response to pathogens. A total of 11 rats underwent sepsis induction and measured systolic, diastolic and mean arterial blood pressure. Leukocyte counts, procalcitonin, and nitric oxide also were measured 0, 2, and 4 hours after the induction of sepsis using the cecal ligation and puncture method. The animals were divided into two groups: control (SHAM) and induced. Procalcitonin levels remained within the normal range for an inflammatory response throughout the experiment. There was a statistically insignificant increase in nitric oxide levels. All animals showed increased diastolic arterial blood pressure; however, the increase in the induced animals was even more pronounced. Procalcitonin and nitric oxide levels can increase due to surgical manipulation, while arterial blood pressure was not a good predictor for the onset of sepsis during the time period studied here.

Sign in / Sign up

Export Citation Format

Share Document