The Renal Prostaglandin System: Localization and Some Biological Effects1

2015 ◽  
pp. 82-91 ◽  
Author(s):  
Carin Lanson
Keyword(s):  
Prostaglandin System

Prostaglandin System and Inflammation

1981 ◽  
pp. 97-108 ◽  
Author(s):  
G. P. Velo ◽  
M. E. Fracasso ◽  
R. Leone ◽  
R. Milanino
Keyword(s):  
Prostaglandin System

Effect of Irradiation on the Prostaglandin System of Human Hypernephroma Cells

1992 ◽  
pp. 53-57
Author(s):  
S. R. Li ◽  
Irene Virgolini ◽  
E. Wandl ◽  
Qiong Yang ◽  
H. Sinzinger
Keyword(s):  
Human Hypernephroma ◽  
Prostaglandin System

scholarly journals Effects of Indomethacin and Ibuprofen on Cerebral Metabolism and Blood Flow in Traumatized Brain

1983 ◽  
Vol 3 (4) ◽  
pp. 448-459 ◽  
Author(s):  
Hanna M. Pappius ◽  
Leonhard S. Wolfe
Keyword(s):  
Blood Flow ◽  
Considerable Increase ◽  
Glucose Utilization ◽  
Single Injection ◽  
Cerebral Metabolism ◽  
Local Cerebral Blood Flow ◽  
Lesion Area ◽  
Local Cerebral Glucose Utilization ◽  
Biphasic Effect ◽  
Prostaglandin System

Local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) were studied by autoradiographic techniques in indomethacin- and ibuprofen-treated rats with focal cortical freezing lesions. Widespread depression of LCGU, which developed with time after the lesion in untreated animals was significantly diminished by the prostaglandin synthetase inhibitors indomethacin (single injection 7.5 mg/kg) and ibuprofen (36 mg/kg/day). Both drugs were effective when given 6 h before or up to 24 h after the lesion was made. The effect of the drugs was most striking in cortical areas of the traumatized hemisphere, where the depression was most profound in untreated animals. Thus, 3 days afer the lesion, average LCGU in these regions was 46%, 86%, and 98% of normal in untreated, indomethacin-pretreated, and ibuprofen-pretreated rats, respectively. Prostaglandin formation was completely inhibited in the lesion area in the indomethacin-treated rats (PGF2α 1.8 ng/g, compared to 57.5 ng/g in untreated and 1.4 ng/g in nonlesioned animals). The results suggest that some components of the prostaglandin system are involved in mechanisms underlying a widespread depression in functional state of the rat brain that develops in response to injury. In control animals, indomethacin was shown to have a biphasic effect on LCBF, an early depression shown previously by others followed at 24 h by a considerable increase.

Characterization of furosemide-induced activation of the renal prostaglandin system

1979 ◽  
Vol 60 (2-3) ◽  
pp. 181-187 ◽  
Author(s):  
Giovanni Ciabattoni ◽  
Francesco Pugliese ◽  
Giulio A. Cinotti ◽  
Giovanni Stirati ◽  
Roberto Ronci ◽  
...  
Keyword(s):  
Prostaglandin System

Prostaglandins and renin release in vitro

1981 ◽  
Vol 240 (6) ◽  
pp. E609-E614
Author(s):  
C. S. Lin ◽  
H. Iwao ◽  
S. Puttkammer ◽  
A. M. Michelakis
Keyword(s):  
Arachidonic Acid ◽  
Renal Cortex ◽  
The Other ◽  
Renin Release ◽  
Eicosatetraenoic Acid ◽  
Juxtaglomerular Cells ◽  
Prostaglandin F2 Alpha ◽  
Prostaglandin System

The present studies were undertaken to explore further the role of prostaglandins in the release of renin from the renal cortex. To provide the best assessment of renin release, renin was determined by a radioimmunoassay for the direct measurement of renin. Slices of mouse renal cortex were incubated at 37 degrees C with arachidonic acid (AA), 5,8,11,14-eicosatetraenoic acid (ETA), indomethacin, prostaglandins, and synthetic prostaglandin endoperoxide analogue (EPA). Our results showed that AA at 1.5 X 10(-8) M significantly increased renin release at 10 and 30 min of incubation. This renin increase ws abolished by either ETA or indomethacin. Prostaglandin F2 alpha (PGF2 alpha) also significantly stimulated renin release at 10 and 60 min. PGE2 and 16,16-dimethyl PGE2 (DMPGE2) showed much less renin release-stimulating activity. EPA and PGI2 on the other hand very strongly stimulated renin release. However, at higher concentrations the stimulating effect of PGI2 and EPA disappeared and even became inhibitory in the case of EPA. Other prostaglandins were found to have no effect on renin release. The results suggest that the prostaglandin system directly affects renin release from the juxtaglomerular cells independent of systemic neurogenic and hemodynamic influences.

Is the cardiovascular effect of nitroglycerin related to the prostaglandin system in the dog?

1983 ◽  
Vol 96 (3-4) ◽  
pp. 285-289 ◽  
Author(s):  
Kazushige Sakai ◽  
Michitaka Akima ◽  
Yasuyuki Nakamura
Keyword(s):  
Cardiovascular Effect ◽  
Prostaglandin System
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