Modulation of NO and endothelin by chronic increases in blood flow in canine femoral arteries

1992 ◽  
Vol 263 (1) ◽  
pp. H103-H108 ◽  
Author(s):  
V. M. Miller ◽  
J. C. Burnett
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pertussis Toxin ◽  
Isometric Force ◽  
Regulatory Proteins ◽  
Arterial Blood Flow ◽  
Guanine Nucleotide ◽  
Femoral Arteries ◽  
Arterial Blood ◽  
Guanine Nucleotide Regulatory Proteins

Experiments were designed to determine whether chronic increases in arterial blood flow alter production of or response to nitric oxide and endothelin. Canine femoral arteries proximal to an arteriovenous fistula- and from the contralateral sham-operated blood vessels were removed, cut into rings, and suspended for measurement of isometric force in organ chambers. The remainder of the artery was homogenized for measurement of endothelin content by radioimmunoassay. NG-monomethyl-L-arginine (10(-4) M) caused concentration-dependent increases in tension only in fistula-operated arteries. Endothelium-dependent relaxations to acetylcholine and BHT-920 were greater in fistula- compared with sham-operated arteries. These differences were reduced by the arginine analogue. Pertussis toxin (100 ng/ml) inhibited relaxations to acetylcholine only in fistula-operated arteries and to BHT-920 only in sham-operated arteries. Contractions to endothelin-1 were greater in fistula- compared with sham-operated arteries. These results suggest that chronic increases in blood flow enhance the tonic and receptor-stimulated production of nitric oxide and its release by receptors coupled to pertussis toxin-sensitive guanine nucleotide regulatory proteins. Furthermore, chronic increases in blood flow may either inhibit the production of endothelin or promote its depletion from endothelial cells while simultaneously increasing the sensitivity of the smooth muscle to its contractile effects.

Progesterone and modulation of endothelium-dependent responses in canine coronary arteries

1991 ◽  
Vol 261 (4) ◽  
pp. R1022-R1027 ◽  
Author(s):  
V. M. Miller ◽  
P. M. Vanhoutte
Keyword(s):  
Nitric Oxide ◽  
Coronary Arteries ◽  
Chronic Treatment ◽  
Isometric Force ◽  
Calcium Ionophore ◽  
Treated Group ◽  
Regulatory Proteins ◽  
Adrenergic Agonist ◽  
Messenger System ◽  
Guanine Nucleotide Regulatory Proteins

Chronic treatment with estrogens enhances some endothelium-dependent relaxations. Whether or not progesterone would exert a similar effect is unknown. Experiments were designed to determine the effect of chronic treatment with progesterone on endothelium-dependent responses. Adult female dogs were ovariectomized and pellets containing carrier substance, estrogen, progesterone, or estrogen plus progesterone were implanted subcutaneously. After 14-21 days coronary arteries were removed, cut into rings, and suspended for the measurement of isometric force in organ chambers in the presence of indomethacin. Endothelium-dependent relaxations to ADP, bradykinin, or the calcium ionophore did not differ among groups. However, relaxations to acetylcholine and to the alpha 2-adrenergic agonist BHT-920 were greater in the estrogen-treated group than in the estrogen plus progesterone-treated group. In rings without endothelium, relaxations to nitric oxide and isoproterenol did not differ among groups. However, relaxations of the smooth muscle to ADP were greater in the progesterone-treated group than in the progesterone plus estrogen group. These results suggest that progesterone alone minimally affects endothelium-dependent responses. However, progesterone seems to antagonize the stimulatory effects of estrogen on two endothelium-dependent responses that are associated with pertussis toxin-sensitive guanine nucleotide regulatory proteins and the production of nitric oxide. These studies suggest that a specific receptor/second messenger system can be modulated by female reproductive steroid hormones.

L-arginine augments nitric oxide production and mesenteric blood flow in ovine endotoxemia

1996 ◽  
Vol 271 (4) ◽  
pp. H1296-H1301
Author(s):  
K. G. Allman ◽  
A. P. Stoddart ◽  
M. M. Kennedy ◽  
J. D. Young
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Nitric Oxide Production ◽  
Mesenteric Blood Flow ◽  
Oxide Production ◽  
Arterial Blood ◽  
Nitrate Concentrations

We studied the effects of administrating the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the nitric oxide precursor, L-arginine, on hemodynamic variables and serum nitrate concentrations in an anesthetized ovine model of endotoxemia to assess the effects on regional visceral blood flow and to determine whether L-arginine availability limits nitric oxide production. Animals received Escherichia coli endotoxin (2 micrograms/kg) followed 2 h later by L-NAME (25 mg/kg), L-arginine (0.575 g/kg), or saline administered over 1 h followed by an infusion of the same dose over 8 h (n = 6 per group). Renal and mesenteric blood flow were measured by placement of electromagnetic flow probes, and serum nitrate concentrations were determined using vanadium III chloride or nitrate reductase reduction to nitric oxide or nitrite, respectively. The results showed L-NAME significantly increased systemic vascular resistance (P < 0.01), decreased serum nitrate concentrations (P < 0.05), and caused a transient reduction in mesenteric blood flow (P < 0.05). L-Arginine caused a reduction in systemic vascular resistance (P < 0.01), increased mesenteric blood flow (P < 0.001) and conductance (P < 0.05). There were no significant changes in renal arterial blood flow in either group. We conclude that the availability of L-arginine limits nitric oxide production in endotoxemia and, furthermore, that L-arginine administration in this model causes significant mesenteric vasodilatation. L-NAME administration had only limited effect on visceral blood flow despite a marked increase in systemic vascular resistance and a reduction in nitric oxide production.

Nitric oxide increases hepatic arterial blood flow in rats with carbon tetrachloride–induced acute hepatic injury

1999 ◽  
Vol 117 (1) ◽  
pp. 173-180 ◽  
Author(s):  
Noriko Tanaka ◽  
Katsuaki Tanaka ◽  
Yoji Nagashima ◽  
Masaaki Kondo ◽  
Hisahiko Sekihara
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Carbon Tetrachloride ◽  
Hepatic Injury ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Acute Hepatic Injury

Nitric oxide signalling is involved in diarylheptanoid-induced increases in femoral arterial blood flow in ovariectomized rats

2013 ◽  
Vol 40 (3) ◽  
pp. 240-249 ◽  
Author(s):  
Ganyapong Chaturapanich ◽  
Rungsima Yamthed ◽  
Pawinee Piyachaturawat ◽  
Arthit Chairoungdua ◽  
Wisuda Suvitayavat ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Arterial Blood Flow ◽  
Ovariectomized Rats ◽  
Arterial Blood

scholarly journals Involvement of nitric oxide in the modulation of dural arterial blood flow in the rat

2000 ◽  
Vol 129 (7) ◽  
pp. 1397-1404 ◽  
Author(s):  
K Messlinger ◽  
A Suzuki ◽  
M Pawlak ◽  
A Zehnter ◽  
R F Schmidt
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Arterial Blood Flow ◽  
Arterial Blood

Importance of nitric oxide in hepatic arterial blood flow and total hepatic blood volume regulation in pigs

1997 ◽  
Vol 161 (3) ◽  
pp. 303-309 ◽  
Author(s):  
F. GRUND ◽  
H. T. SOMMERSCHILD ◽  
A. WINECOFF ◽  
M. R. UJHELYI ◽  
T. TØNNESSEN ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Blood Volume ◽  
Volume Regulation ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood

Microvascular oxygenation, oxidative stress, NO suppression and superoxide dismutase during postischemic reperfusion

2003 ◽  
Vol 285 (3) ◽  
pp. H1064-H1071 ◽  
Author(s):  
S. Bertuglia ◽  
A. Giusti
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Flow ◽  
Leukocyte Adhesion ◽  
Arterial Blood Flow ◽  
Cheek Pouch ◽  
Ros Production ◽  
Early Reperfusion ◽  
Postischemic Reperfusion ◽  
Arterial Blood

Increased formation of reactive oxygen species (ROS) on reperfusion after ischemia underlies ischemia-reperfusion (I/R) damage. We measured, in real time, oxygen tension in both microvessels and tissue and oxidant stress during postischemic reperfusion in the hamster cheek pouch microcirculation. We measured Po2 by using phosphorescence quenching microscopy and ROS production in the systemic blood. We evaluated the effects of a nitric oxide synthase inhibitor ( NG-monomethyl-l-arginine, l-NMMA) and SOD on the oxidative stress during reperfusion. Microvascular injury was assessed by measuring diameter change, the perfused capillary length (PCL), and leukocyte adhesion. During early reperfusion, arteriolar Po2 was significantly lower than baseline, whereas capillary Po2 varied between 7 and 0 mmHg. Arterial blood flow did not regain baseline values, whereas Po2 returned to baseline in arterioles and tissue after 30 min of reperfusion. During 5 and 15 min of reperfusion, ROS increased by 72 and 89% versus baseline, respectively, and declined to baseline after 30 min of reperfusion. Pretreatment with SOD maintained ROS at normal levels, increased arteriolar diameter, blood flow, and PCL, and decreased leukocyte adhesion ( P < 0.05). l-NMMA decreased ROS only within 5 min of reperfusion, which increased significantly by 72% later during reperfusion. l-NMMA worsened leukocyte adhesion ( P < 0.05). In conclusion, our results show that the early reperfusion is characterized by low Po2 linked to increased production of ROS. At early reperfusion both SOD and l-NMMA decreased ROS production, whereas only SOD reduced it during later reperfusion. We suggest that low-flow hypoxia profoundly affects vascular endothelial damage during reperfusion through changes in ROS and nitric oxide production.

scholarly journals Role of guanine nucleotide regulatory proteins in insulin stimulation of glucose transport in rat adipocytes. Influence of bacterial toxins

1989 ◽  
Vol 264 (2) ◽  
pp. 389-396 ◽  
Author(s):  
T P Ciaraldi ◽  
A Maisel
Keyword(s):  
Glucose Transport ◽  
Pertussis Toxin ◽  
Insulin Binding ◽  
Regulatory Proteins ◽  
Guanine Nucleotide ◽  
Insulin Stimulation ◽  
Guanine Nucleotide Regulatory Proteins ◽  
Toxin Inhibition ◽  
Stimulation Of

The potential role of guanine nucleotide regulatory proteins (G-proteins) in acute insulin regulation of glucose transport was investigated by using bacterial toxins which are known to modify these proteins. Cholera-toxin treatment of isolated rat adipocytes had no effect on either 2-deoxyglucose transport or insulin binding. Pertussis-toxin treatment resulted in an inhibition of both insulin binding and glucose transport. Insulin binding was decreased in pertussis-toxin-treated cells by up to 40%, owing to a lowering of the affinity of the receptor for hormone, with no change in hormone internalization. The dose-response curve for insulin stimulation of glucose transport was strongly shifted to the right by pertussis-toxin treatment [EC50 (half-maximally effective insulin concn.) = 0.31 +/- 0.04 ng/ml in control cells; 2.29 +/- 1.0 in treated cells), whereas cholera toxin had only a small effect (EC50 = 0.47 +/- 0.02 ng/ml). Correcting for the change in hormone binding, pertussis toxin was found to decrease the coupling efficiency of occupied receptors (50% of maximal insulin effect with 928 molecules bound/cell in control and 3418 in treated cells). Pertussis-toxin inhibition of insulin sensitivity was slow in onset, requiring 2-3 h for completion. Under conditions where pertussis-toxin inhibition of insulin sensitivity was maximal, a 41,000 Da protein similar to the alpha subunit of Gi (the inhibitory G-protein) was found to be fully ribosylated. These results are consistent with the concept that pertussis-toxin-sensitive G-protein(s) can modify the insulin-receptor/glucose-transport coupling system.

Sign in / Sign up

Export Citation Format

Share Document