scholarly journals Reduced capacity of tumour blood vessels to produce endothelium-derived relaxing factor: significance for blood flow modification

1996 ◽  
Vol 74 (12) ◽  
pp. 1955-1960 ◽  
Author(s):  
GM Tozer ◽  
VE Prise ◽  
KM Bell ◽  
MF Dennis ◽  
MRL Stratford ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Flow Modification ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Tumour Blood

Enhanced release of endothelium-derived factor(s) by chronic increases in blood flow

1988 ◽  
Vol 255 (3) ◽  
pp. H446-H451 ◽  
Author(s):  
V. M. Miller ◽  
P. M. Vanhoutte
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Arteriovenous Fistula ◽  
Muscarinic Receptors ◽  
Femoral Artery ◽  
Response Curves ◽  
Femoral Arteries ◽  
Relaxing Factor ◽  
Bioassay System ◽  
Endothelium Derived Relaxing Factor

Chronic increases in blood flow caused by an arteriovenous fistula augment endothelium-dependent relaxations to acetylcholine. To determine whether endothelial muscarinic receptors are altered, concentration-response curves to acetylcholine were obtained in the presence of pirenzepine in fistula- and sham-operated canine femoral arteries. Pirenzepine inhibited the response to acetylcholine in both arteries. The pA2 (log Kb) for the antagonist was the same. A bioassay system was used to assess release of endothelium-derived relaxing factor. Rings of femoral artery (without endothelium) from unoperated dogs relaxed more when superfused with perfusate derived from endothelium of fistula-operated arteries during acetylcholine stimulation. Rings without endothelium of sham- and fistula-operated arteries relaxed to the same extent when superfused with perfusate derived from the endothelium of unoperated femoral arteries. These results suggest that augmented relaxations to acetylcholine in canine arteries where blood flow is chronically elevated do not result from changes in the subtype of endothelial muscarinic receptors or in the sensitivity of the underlying smooth muscle to endothelium-derived relaxing factor(s). They are likely due to increased release of endothelium-derived relaxing factor(s) on muscarinic activation.

Glucocorticoid-induced renal vasodilatation is mediated by a direct renal action involving nitric oxide

1997 ◽  
Vol 273 (6) ◽  
pp. R1972-R1979 ◽  
Author(s):  
R. De Matteo ◽  
C. N. May
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Plasma Cortisol ◽  
Filtration Rate ◽  
Systemic Effects ◽  
Renal Vasculature ◽  
Relaxing Factor ◽  
Renal Action ◽  
Endothelium Derived Relaxing Factor ◽  
Conscious Sheep

Glucocorticoids increase renal blood flow (RBF) and glomerular filtration rate, but the mechanisms are unclear. We investigated whether the cortisol-induced increment in RBF is a direct renal action or secondary to its systemic effects and whether nitric oxide (NO) plays a role in this response. In conscious sheep, cortisol infused intravenously (5.0 mg/h) or into the renal artery (1.3 mg/h) for 5 h increased RBF by 66 ± 8 and 53 ± 11 ml/min, respectively. Plasma glucose was increased by intravenous cortisol (0.4 ± 0.1 mmol/l) but not by intrarenal cortisol. Renal vein plasma cortisol levels were similar at the end of each infusion (193 ± 31 intravenously; 151 ± 25 nmol/l intrarenal), but systemic levels were different (277 ± 31 intravenous; 69 ± 10 nmol/l intrarenal). Inhibition of NO synthesis by N ω-nitro-l-arginine infused intravenously (10 mg/kg followed by 5 mg ⋅ kg−1 ⋅ h−1) or intrarenally (2 mg ⋅ kg−1 ⋅ h−1) significantly reduced the cortisol-induced renal vasodilatation. In contrast, constriction of the renal vasculature with intrarenal angiotensin (0.3 μg/h) did not prevent the cortisol-induced renal vasodilatation. These findings demonstrate that cortisol acts directly on the kidney to cause renal vasodilatation and to increase RBF and suggest that this response involves the endothelium-derived relaxing factor NO.

Influence of endothelium-derived relaxing factor on renal microvessels and pressure-dependent vasodilation

1993 ◽  
Vol 265 (2) ◽  
pp. F285-F292 ◽  
Author(s):  
J. Hoffend ◽  
A. Cavarape ◽  
K. Endlich ◽  
M. Steinhausen
Keyword(s):  
Blood Flow ◽  
Renal Perfusion ◽  
Local Administration ◽  
Relaxing Factor ◽  
Female Wistar Rats ◽  
Stepwise Reduction ◽  
Afferent Arterioles ◽  
Endothelium Derived Relaxing Factor ◽  
Hydronephrotic Kidney

The influence of endothelium-derived relaxing factor (EDRF) on renal microvessels and autoregulation was visualized in vivo, in the split hydronephrotic kidney of rats. EDRF synthesis was inhibited by local administration of 10(-5) M NG-nitro-L-arginine methyl ester (L-NAME). Diameters of arcuate arteries decreased by 17%. In cortical vessels efferent arterioles constricted more (13-16%) than interlobular arteries and afferent arterioles (7-12%). Cortical glomerular blood flow (GBF) decreased by 46% after L-NAME. A similar behavior of blood flow and vascular diameters was also observed in juxtamedullary (JM) arterioles. The responses to acetylcholine but not to sodium nitroprusside were attenuated after L-NAME. After local administration of L-arginine (10(-3) M) diameters of all vessels and GBF increased, vascular responses to L-NAME were blunted. Stepwise reduction of renal perfusion pressure revealed that autoregulation was preserved in cortical vessels after L-NAME. In JM arterioles, which do not autoregulate in female Wistar rats, autoregulation of GBF was enhanced after L-NAME. These data suggest that tonic formation of EDRF influences basal renal hemodynamics to a considerable extent. EDRF may also impair autoregulation of JM glomeruli without disturbing autoregulation of cortical glomeruli.

Endotoxin-induced alterations in contractility of isolated blood vessels from sheep

1991 ◽  
Vol 260 (6) ◽  
pp. H1790-H1794 ◽  
Author(s):  
S. Nelson ◽  
R. H. Steward ◽  
L. Traber ◽  
D. Traber
Keyword(s):  
Escherichia Coli ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Blood Vessels ◽  
Femoral Artery ◽  
Vascular Reactivity ◽  
Relaxing Factor ◽  
Tertiary Branch ◽  
Endothelium Derived Relaxing Factor ◽  
And Control

The present study examined reactivity to norepinephrine (NE) and KCl in isolated, suffused blood vessels from the systemic and pulmonary circulations of endotoxin-treated and control sheep. A possible mechanism underlying an endotoxin-induced alteration in vascular reactivity was also investigated. Chronically instrumented sheep were given Escherichia coli endotoxin (1.5 micrograms/kg). Eight to 12 h later these endotoxin-treated animals exhibited a significantly increased cardiac output and decreased systemic vascular pressure and resistance. The pulmonary vascular pressure and resistance were not changed. The isolated superficial femoral artery from the endotoxin sheep exhibited depressed contractions in response to KCl (75 mM) and to NE (10(-7)-10(-5) M), whereas the pulmonary artery (tertiary branch) did not exhibit altered reactivity. The decreased sensitivity to NE in the femoral artery from endotoxin sheep did not appear to involve an alteration of alpha- or beta-adrenoceptors, or an increased release of vasodilator prostanoids, or endothelium-derived relaxing factor.

Increasing oxygen tension dilates fetal pulmonary circulation via endothelium-derived relaxing factor

1993 ◽  
Vol 265 (1) ◽  
pp. H376-H380 ◽  
Author(s):  
M. H. Tiktinsky ◽  
F. C. Morin
Keyword(s):  
Blood Flow ◽  
Oxygen Tension ◽  
Hyperbaric Oxygen ◽  
Pulmonary Circulation ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Absolute Pressure ◽  
Relaxing Factor ◽  
Pulmonary Arterial ◽  
Endothelium Derived Relaxing Factor

We examined the role of endothelium-derived relaxing factor (EDRF) in the increase in pulmonary blood flow caused by increasing oxygen tension in the lungs of the fetus. Fetal lambs at 133 days of gestation were instrumented for intrauterine measurement of pulmonary arterial, left atrial, and amniotic fluid pressure and pulmonary blood flow. Three days later oxygen tension in the pulmonary arterial blood of the fetus was doubled by having the ewe breathe 100% oxygen at 3 atm absolute pressure. In the control fetuses (n = 5), hyperbaric oxygenation increased pulmonary blood flow eightfold. Blocking EDRF production by infusing 45 mg of NG-monomethyl-L-arginine into the superior vena cava of the fetus over 5 min starting 30 min after the beginning of hyperbaric oxygen reversed the increase in pulmonary blood flow (n = 5). Blocking EDRF production by infusing NG-nitro-L-arginine at 1 mg/min for 60 min starting 30 min before hyperbaric oxygen blunted the initial increase in pulmonary blood flow and eliminated it by the end of the experiment (n = 5). As hyperbaric oxygen did not significantly alter pulmonary arterial or left atrial pressure, changes in pulmonary vascular conductance paralleled those in pulmonary blood flow. We conclude that the majority of the vasodilation of the fetal pulmonary circulation caused by increasing oxygen tension is mediated by EDRF. We speculate that EDRF is involved in maintaining low vascular tone at the relatively high oxygen tension of the postnatal lung.

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